stat1  (Taconic Biosciences)

 
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    Name:
    Stat1
    Description:
    Contains a homozygous disruption of the Stat1 gene and complete lack of functional STAT1 proteins The JAK STAT signaling pathway has been implicated in mediating biologic responses induced by many cytokines Homozygous mice develop normally Deficient immune cell response to alpha α and gamma γ interferons Extreme susceptibility to infections by microbial pathogens and viruses Could be used as sentinel animals for evaluating the health status of a mouse colony Accelerated and amplified development of chemically induced and spontaneous tumors Useful in determining the role of a variety of cytokines in immune responses the role of STAT1 protein in mediating interferon dependent responses and the roles of tumor cells and immune cells in mediating tumor cell destruction
    Catalog Number:
    2045-f
    Price:
    None
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    Structured Review

    Taconic Biosciences stat1
    <t>STAT1-activating</t> cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Contains a homozygous disruption of the Stat1 gene and complete lack of functional STAT1 proteins The JAK STAT signaling pathway has been implicated in mediating biologic responses induced by many cytokines Homozygous mice develop normally Deficient immune cell response to alpha α and gamma γ interferons Extreme susceptibility to infections by microbial pathogens and viruses Could be used as sentinel animals for evaluating the health status of a mouse colony Accelerated and amplified development of chemically induced and spontaneous tumors Useful in determining the role of a variety of cytokines in immune responses the role of STAT1 protein in mediating interferon dependent responses and the roles of tumor cells and immune cells in mediating tumor cell destruction
    https://www.bioz.com/result/stat1/product/Taconic Biosciences
    Average 96 stars, based on 35 article reviews
    Price from $9.99 to $1999.99
    stat1 - by Bioz Stars, 2020-11
    96/100 stars

    Images

    1) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    2) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    3) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    4) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    5) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    6) Product Images from "Suppression of GM-CSF expression in murine and human T cells by IL-27"

    Article Title: Suppression of GM-CSF expression in murine and human T cells by IL-27

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1200131

    Suppression of GM-CSF expression by IL-27 is independent of IL-10, IL-2, IFN-γ and SOCS3 signalling but dependent on Jak2/Tyk2 activity and STAT1 signalling
    Figure Legend Snippet: Suppression of GM-CSF expression by IL-27 is independent of IL-10, IL-2, IFN-γ and SOCS3 signalling but dependent on Jak2/Tyk2 activity and STAT1 signalling

    Techniques Used: Expressing, Activity Assay

    7) Product Images from "IL-4 confers resistance to IL-27-mediated suppression on CD4+ T cells by impairing STAT1 signaling"

    Article Title: IL-4 confers resistance to IL-27-mediated suppression on CD4+ T cells by impairing STAT1 signaling

    Journal: The Journal of allergy and clinical immunology

    doi: 10.1016/j.jaci.2013.06.035

    The high concentrations of Th2-inducing reagents specifically impair STAT1 phosphorylation. A-B , Intracellular staining of IL-4 and IFN-γ protein in cells primed Th2 int conditions for 5 days. C , Western analysis of STAT1 phosphorylation in cultured
    Figure Legend Snippet: The high concentrations of Th2-inducing reagents specifically impair STAT1 phosphorylation. A-B , Intracellular staining of IL-4 and IFN-γ protein in cells primed Th2 int conditions for 5 days. C , Western analysis of STAT1 phosphorylation in cultured

    Techniques Used: Staining, Western Blot, Cell Culture

    STAT1 phosphorylation is inhibited in memory Th2 cells of allergic asthmatic patients. A , FACS analysis of STAT1 phosphorylation (pSTAT1) in various subsets of CD4 + T cells. Naïve=naïve CD4 + T cells; Th2 m =memory Th2 cells; non-Th2 m =memory
    Figure Legend Snippet: STAT1 phosphorylation is inhibited in memory Th2 cells of allergic asthmatic patients. A , FACS analysis of STAT1 phosphorylation (pSTAT1) in various subsets of CD4 + T cells. Naïve=naïve CD4 + T cells; Th2 m =memory Th2 cells; non-Th2 m =memory

    Techniques Used: FACS

    8) Product Images from "IFN-γ prevents adenosine receptor (A2bR) upregulation to sustain the macrophage activation response"

    Article Title: IFN-γ prevents adenosine receptor (A2bR) upregulation to sustain the macrophage activation response

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1501139

    IFN-γ preferentially inhibits LPS-induced A2bR expression in macrophages (A) mRNA expression of A1r (dotted bars), A2ar (horizontally striped bars), A2br (diagonally striped bars), and A3r (solid black bars) in unprimed and IFN-γ primed BMDMs stimulated for 4 hours. The means +/− SEM of 3 independent experiments are shown. (B,D) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with the indicated TLR agonists for 4 hours. A2bR (B) and A2aR (D) mRNA levels were determined by qPCR. The means +/−SEM of at least 3 independent determinations are shown. (C) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with LPS over time. A2bR mRNA levels were determined by qPCR. The means +/−SEM of 2 independent experiments are shown. (D) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with the indicated TLR agonists for 4hrs. A2aR mRNA levels were determined by qPCR. The means +/−SEM of at least 3 independent determinations are shown. (E) WT BMDMs (black bars) or STAT1 −/− BMDMs (striped bars) were left unprimed or IFN-γ primed, then stimulated with LPS for 4 hours. A2bR mRNA levels were determined by qPCR. The mean +/−SEM of at least 3 independent determinations are shown.
    Figure Legend Snippet: IFN-γ preferentially inhibits LPS-induced A2bR expression in macrophages (A) mRNA expression of A1r (dotted bars), A2ar (horizontally striped bars), A2br (diagonally striped bars), and A3r (solid black bars) in unprimed and IFN-γ primed BMDMs stimulated for 4 hours. The means +/− SEM of 3 independent experiments are shown. (B,D) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with the indicated TLR agonists for 4 hours. A2bR (B) and A2aR (D) mRNA levels were determined by qPCR. The means +/−SEM of at least 3 independent determinations are shown. (C) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with LPS over time. A2bR mRNA levels were determined by qPCR. The means +/−SEM of 2 independent experiments are shown. (D) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with the indicated TLR agonists for 4hrs. A2aR mRNA levels were determined by qPCR. The means +/−SEM of at least 3 independent determinations are shown. (E) WT BMDMs (black bars) or STAT1 −/− BMDMs (striped bars) were left unprimed or IFN-γ primed, then stimulated with LPS for 4 hours. A2bR mRNA levels were determined by qPCR. The mean +/−SEM of at least 3 independent determinations are shown.

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction

    IFN-γ prolongs the macrophage activation state (A,C) Cytokine production by LPS stimulated unprimed (black squares, solid line) or IFN- γ primed (gray circles, solid line) BMDMs over time. TNFα (A) and IL-12/23p40 (C) was detected by ELISA. The means +/− SEM of 3 independent experiments are shown. (B,D) Unprimed (black squares, solid line) or IFN- γ primed (gray circles, solid line) BMDMs were stimulated with LPS then washed with PBS (break in y-axis) and replaced with LPS-free media and monitored over the next 1–6 hours for TNFα (B), IL-12/23p40 (D). (E) BMDMs were stimulated with LPS alone or in the presence of increasing doses of POM-1. 8 hours post stimulation, cytokine production was assessed by ELISA for TNFα (blue line), IL-12/23p40 (red line), and IL-10 (black line). The means +/− SEM of 3 experiments are shown. (F–I) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with LPS for 4 hrs. Il-10 (F), Arg1 (G), Il-33 (H), and Hmox-1 (I) mRNA levels were determined by qPCR. The means +/−SEM of at least 3 independent experiments are shown. (J) WT (black bars) or STAT1 −/− BMDMs (striped bars) were left unprimed or primed with IFN-γ then stimulated with LPS. TNFα (left) and IL-12/23p40 (right) were measured in the supernatants 8 hours after stimulation. Protein was measured by ELISA. The means +/− SD of triplicates are shown.
    Figure Legend Snippet: IFN-γ prolongs the macrophage activation state (A,C) Cytokine production by LPS stimulated unprimed (black squares, solid line) or IFN- γ primed (gray circles, solid line) BMDMs over time. TNFα (A) and IL-12/23p40 (C) was detected by ELISA. The means +/− SEM of 3 independent experiments are shown. (B,D) Unprimed (black squares, solid line) or IFN- γ primed (gray circles, solid line) BMDMs were stimulated with LPS then washed with PBS (break in y-axis) and replaced with LPS-free media and monitored over the next 1–6 hours for TNFα (B), IL-12/23p40 (D). (E) BMDMs were stimulated with LPS alone or in the presence of increasing doses of POM-1. 8 hours post stimulation, cytokine production was assessed by ELISA for TNFα (blue line), IL-12/23p40 (red line), and IL-10 (black line). The means +/− SEM of 3 experiments are shown. (F–I) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with LPS for 4 hrs. Il-10 (F), Arg1 (G), Il-33 (H), and Hmox-1 (I) mRNA levels were determined by qPCR. The means +/−SEM of at least 3 independent experiments are shown. (J) WT (black bars) or STAT1 −/− BMDMs (striped bars) were left unprimed or primed with IFN-γ then stimulated with LPS. TNFα (left) and IL-12/23p40 (right) were measured in the supernatants 8 hours after stimulation. Protein was measured by ELISA. The means +/− SD of triplicates are shown.

    Techniques Used: Activation Assay, Enzyme-linked Immunosorbent Assay, Real-time Polymerase Chain Reaction

    9) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    10) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    11) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    12) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    13) Product Images from "Replication of Norovirus in Cell Culture Reveals a Tropism for Dendritic Cells and MacrophagesNorovirus Cultured for the First Time"

    Article Title: Replication of Norovirus in Cell Culture Reveals a Tropism for Dendritic Cells and MacrophagesNorovirus Cultured for the First Time

    Journal: PLoS Biology

    doi: 10.1371/journal.pbio.0020432

    MNV-1-Specific Staining In Vivo Occurs in Cells of the MΦ Lineage Immunohistochemistry was performed on liver (A and B) and spleen (C and D) sections from STAT1 −/− mice 2 d after oral infection. MNV-1-specific staining was seen in Kupffer cells of infected livers when probed with MNV-1 immune (A) but not preimmune (B) serum. A selected Kupffer cell lining the sinusoid is indicated by an arrowhead. MNV-1-specific staining consistent with MΦ was seen in red pulp (C) and marginal zone (D) in the spleen. The arrow indicates a cell with MΦ morphology. No staining was observed in tissues from mice infected for 1 d, in infected tissues incubated with preimmune serum, or in mock-infected tissues incubated with immune serum. RP, red pulp; WP, white pulp.
    Figure Legend Snippet: MNV-1-Specific Staining In Vivo Occurs in Cells of the MΦ Lineage Immunohistochemistry was performed on liver (A and B) and spleen (C and D) sections from STAT1 −/− mice 2 d after oral infection. MNV-1-specific staining was seen in Kupffer cells of infected livers when probed with MNV-1 immune (A) but not preimmune (B) serum. A selected Kupffer cell lining the sinusoid is indicated by an arrowhead. MNV-1-specific staining consistent with MΦ was seen in red pulp (C) and marginal zone (D) in the spleen. The arrow indicates a cell with MΦ morphology. No staining was observed in tissues from mice infected for 1 d, in infected tissues incubated with preimmune serum, or in mock-infected tissues incubated with immune serum. RP, red pulp; WP, white pulp.

    Techniques Used: Staining, In Vivo, Immunohistochemistry, Mouse Assay, Infection, Incubation

    MNV-1 from Brain Homogenate Replicates in Cells of the DC and MΦ Lineage In Vitro BMDCs and BMMΦ, as well as MEFs from wt or STAT1 −/− mice, and RAW 264.7 cells were infected with a MOI of 0.05. (A) MNV-1 causes CPE in permissive cells. MNV-1- or mock-infected cells were observed by light microscopy 2 d postinfection. The boxed area is magnified further to show the border of the plaque. (B) Infected cell lysates were analyzed in two to four independent experiments by plaque assay at various timepoints postinfection to calculate standard deviations. For wt BMMΦ, MNV-1 growth was detected in two out of four experiments.
    Figure Legend Snippet: MNV-1 from Brain Homogenate Replicates in Cells of the DC and MΦ Lineage In Vitro BMDCs and BMMΦ, as well as MEFs from wt or STAT1 −/− mice, and RAW 264.7 cells were infected with a MOI of 0.05. (A) MNV-1 causes CPE in permissive cells. MNV-1- or mock-infected cells were observed by light microscopy 2 d postinfection. The boxed area is magnified further to show the border of the plaque. (B) Infected cell lysates were analyzed in two to four independent experiments by plaque assay at various timepoints postinfection to calculate standard deviations. For wt BMMΦ, MNV-1 growth was detected in two out of four experiments.

    Techniques Used: In Vitro, Mouse Assay, Infection, Light Microscopy, Plaque Assay

    Changes in Virulence of Plaque-Purified MNV-1 over Multiple Passages Are Associated with Limited Amino Acid Changes (A) Serial passage of MNV-1.CW1 in cell culture causes attenuation. STAT1 −/− mice were infected orally with the indicated virus dose. The number of mice analyzed is indicated in parentheses. (B) Summary of sequence analysis of MNV-1 over several passages. The nucleotide and amino acid differences between the indicated viruses are shown (for detail see Table 1 ).
    Figure Legend Snippet: Changes in Virulence of Plaque-Purified MNV-1 over Multiple Passages Are Associated with Limited Amino Acid Changes (A) Serial passage of MNV-1.CW1 in cell culture causes attenuation. STAT1 −/− mice were infected orally with the indicated virus dose. The number of mice analyzed is indicated in parentheses. (B) Summary of sequence analysis of MNV-1 over several passages. The nucleotide and amino acid differences between the indicated viruses are shown (for detail see Table 1 ).

    Techniques Used: Purification, Cell Culture, Mouse Assay, Infection, Sequencing

    14) Product Images from "Activation of invariant natural killer T cells impedes liver regeneration via both IFN-γ- and IL-4-dependent mechanisms"

    Article Title: Activation of invariant natural killer T cells impedes liver regeneration via both IFN-γ- and IL-4-dependent mechanisms

    Journal: Hepatology (Baltimore, Md.)

    doi: 10.1002/hep.27128

    The inhibitory effect of α-GalCer on PHx-induced liver regeneration is partially diminished in IFN-γ −/− and STAT1 −/− mice
    Figure Legend Snippet: The inhibitory effect of α-GalCer on PHx-induced liver regeneration is partially diminished in IFN-γ −/− and STAT1 −/− mice

    Techniques Used: Mouse Assay

    15) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    16) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    17) Product Images from "Irf8-Regulated Genomic Responses Drive Pathological Inflammation during Cerebral Malaria"

    Article Title: Irf8-Regulated Genomic Responses Drive Pathological Inflammation during Cerebral Malaria

    Journal: PLoS Pathogens

    doi: 10.1371/journal.ppat.1003491

    IRF8-regulated pro-inflammatory networks commonly activated during cerebral malaria and pulmonary tuberculosis. Networks were generated for the 53 genes up-regulated in B6 mice by both infections which also possess an IRF8 binding site within 20 kb of the TSS (see Table S2 for details). (A) Top scoring network highlighting IRF signaling and MHC class I antigen presentation with gene circles colored according to fold change during PbA infection in B6 d7/d0 (left), BXH2 d7/d0 (center) and M. tuberculosis infection in B6 d30/d0 (right). (B) Second top scoring network highlights Ifng and Stat1 signaling. (C) Third top scoring network highlights MHC Class II and Fc receptors. Genes included in the list of 53 are represented by black circles, while networked genes added by the software are outlined in gray. IRF8-bound genes are outlined in light blue. Direct (black) and indirect (gray) connections between genes are shown by arrows.
    Figure Legend Snippet: IRF8-regulated pro-inflammatory networks commonly activated during cerebral malaria and pulmonary tuberculosis. Networks were generated for the 53 genes up-regulated in B6 mice by both infections which also possess an IRF8 binding site within 20 kb of the TSS (see Table S2 for details). (A) Top scoring network highlighting IRF signaling and MHC class I antigen presentation with gene circles colored according to fold change during PbA infection in B6 d7/d0 (left), BXH2 d7/d0 (center) and M. tuberculosis infection in B6 d30/d0 (right). (B) Second top scoring network highlights Ifng and Stat1 signaling. (C) Third top scoring network highlights MHC Class II and Fc receptors. Genes included in the list of 53 are represented by black circles, while networked genes added by the software are outlined in gray. IRF8-bound genes are outlined in light blue. Direct (black) and indirect (gray) connections between genes are shown by arrows.

    Techniques Used: Generated, Mouse Assay, Binding Assay, Infection, Software

    Effect of deletion of Ifng , Stat1 , Jak3 , Irf1 , Irgm1 , Il12p40 , Ifit1 , Isg15 and Nlrc4 on susceptibility to PbA induced cerebral malaria. Control and mutant mice were infected with 10 6 P. berghei parasites and survival was monitored. Cerebral malaria susceptible mice succumbed between d5 and d10 post-infection with neurological symptoms, while no mice that survived longer than 13 days developed signs of ECM and these were categorized as resistant. Infection specific B6 and BXH2 controls (n > 5 per infection) are plotted alongside each mutant strain.
    Figure Legend Snippet: Effect of deletion of Ifng , Stat1 , Jak3 , Irf1 , Irgm1 , Il12p40 , Ifit1 , Isg15 and Nlrc4 on susceptibility to PbA induced cerebral malaria. Control and mutant mice were infected with 10 6 P. berghei parasites and survival was monitored. Cerebral malaria susceptible mice succumbed between d5 and d10 post-infection with neurological symptoms, while no mice that survived longer than 13 days developed signs of ECM and these were categorized as resistant. Infection specific B6 and BXH2 controls (n > 5 per infection) are plotted alongside each mutant strain.

    Techniques Used: Mutagenesis, Mouse Assay, Infection

    18) Product Images from "Herpes Simplex Virus 2 ICP0− Mutant Viruses Are Avirulent and Immunogenic: Implications for a Genital Herpes Vaccine"

    Article Title: Herpes Simplex Virus 2 ICP0− Mutant Viruses Are Avirulent and Immunogenic: Implications for a Genital Herpes Vaccine

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0012251

    HSV-2 ICP0 − mutant viruses are repressed by a Stat 1-dependent host response. ( A–C ) Viral shedding on Day 2 p.i. from the eyes of (A) wild-type strain 129 mice, (B) lymphocyte-deficient rag2 −/− mice, or (C) IFN-signaling-deficient stat1 −/− mice inoculated bilaterally with 100,000 pfu/eye of wild-type HSV-2 MS, HSV-2 0ΔNLS, or HSV-2 0ΔRING (n = 10 mice per group). A single asterisk (*) denotes p
    Figure Legend Snippet: HSV-2 ICP0 − mutant viruses are repressed by a Stat 1-dependent host response. ( A–C ) Viral shedding on Day 2 p.i. from the eyes of (A) wild-type strain 129 mice, (B) lymphocyte-deficient rag2 −/− mice, or (C) IFN-signaling-deficient stat1 −/− mice inoculated bilaterally with 100,000 pfu/eye of wild-type HSV-2 MS, HSV-2 0ΔNLS, or HSV-2 0ΔRING (n = 10 mice per group). A single asterisk (*) denotes p

    Techniques Used: Mutagenesis, Mouse Assay, Mass Spectrometry

    19) Product Images from "IFN-γ prevents adenosine receptor (A2bR) upregulation to sustain the macrophage activation response"

    Article Title: IFN-γ prevents adenosine receptor (A2bR) upregulation to sustain the macrophage activation response

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1501139

    IFN-γ preferentially inhibits LPS-induced A2bR expression in macrophages (A) mRNA expression of A1r (dotted bars), A2ar (horizontally striped bars), A2br (diagonally striped bars), and A3r (solid black bars) in unprimed and IFN-γ primed BMDMs stimulated for 4 hours. The means +/− SEM of 3 independent experiments are shown. (B,D) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with the indicated TLR agonists for 4 hours. A2bR (B) and A2aR (D) mRNA levels were determined by qPCR. The means +/−SEM of at least 3 independent determinations are shown. (C) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with LPS over time. A2bR mRNA levels were determined by qPCR. The means +/−SEM of 2 independent experiments are shown. (D) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with the indicated TLR agonists for 4hrs. A2aR mRNA levels were determined by qPCR. The means +/−SEM of at least 3 independent determinations are shown. (E) WT BMDMs (black bars) or STAT1 −/− BMDMs (striped bars) were left unprimed or IFN-γ primed, then stimulated with LPS for 4 hours. A2bR mRNA levels were determined by qPCR. The mean +/−SEM of at least 3 independent determinations are shown.
    Figure Legend Snippet: IFN-γ preferentially inhibits LPS-induced A2bR expression in macrophages (A) mRNA expression of A1r (dotted bars), A2ar (horizontally striped bars), A2br (diagonally striped bars), and A3r (solid black bars) in unprimed and IFN-γ primed BMDMs stimulated for 4 hours. The means +/− SEM of 3 independent experiments are shown. (B,D) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with the indicated TLR agonists for 4 hours. A2bR (B) and A2aR (D) mRNA levels were determined by qPCR. The means +/−SEM of at least 3 independent determinations are shown. (C) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with LPS over time. A2bR mRNA levels were determined by qPCR. The means +/−SEM of 2 independent experiments are shown. (D) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with the indicated TLR agonists for 4hrs. A2aR mRNA levels were determined by qPCR. The means +/−SEM of at least 3 independent determinations are shown. (E) WT BMDMs (black bars) or STAT1 −/− BMDMs (striped bars) were left unprimed or IFN-γ primed, then stimulated with LPS for 4 hours. A2bR mRNA levels were determined by qPCR. The mean +/−SEM of at least 3 independent determinations are shown.

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction

    IFN-γ prolongs the macrophage activation state (A,C) Cytokine production by LPS stimulated unprimed (black squares, solid line) or IFN- γ primed (gray circles, solid line) BMDMs over time. TNFα (A) and IL-12/23p40 (C) was detected by ELISA. The means +/− SEM of 3 independent experiments are shown. (B,D) Unprimed (black squares, solid line) or IFN- γ primed (gray circles, solid line) BMDMs were stimulated with LPS then washed with PBS (break in y-axis) and replaced with LPS-free media and monitored over the next 1–6 hours for TNFα (B), IL-12/23p40 (D). (E) BMDMs were stimulated with LPS alone or in the presence of increasing doses of POM-1. 8 hours post stimulation, cytokine production was assessed by ELISA for TNFα (blue line), IL-12/23p40 (red line), and IL-10 (black line). The means +/− SEM of 3 experiments are shown. (F–I) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with LPS for 4 hrs. Il-10 (F), Arg1 (G), Il-33 (H), and Hmox-1 (I) mRNA levels were determined by qPCR. The means +/−SEM of at least 3 independent experiments are shown. (J) WT (black bars) or STAT1 −/− BMDMs (striped bars) were left unprimed or primed with IFN-γ then stimulated with LPS. TNFα (left) and IL-12/23p40 (right) were measured in the supernatants 8 hours after stimulation. Protein was measured by ELISA. The means +/− SD of triplicates are shown.
    Figure Legend Snippet: IFN-γ prolongs the macrophage activation state (A,C) Cytokine production by LPS stimulated unprimed (black squares, solid line) or IFN- γ primed (gray circles, solid line) BMDMs over time. TNFα (A) and IL-12/23p40 (C) was detected by ELISA. The means +/− SEM of 3 independent experiments are shown. (B,D) Unprimed (black squares, solid line) or IFN- γ primed (gray circles, solid line) BMDMs were stimulated with LPS then washed with PBS (break in y-axis) and replaced with LPS-free media and monitored over the next 1–6 hours for TNFα (B), IL-12/23p40 (D). (E) BMDMs were stimulated with LPS alone or in the presence of increasing doses of POM-1. 8 hours post stimulation, cytokine production was assessed by ELISA for TNFα (blue line), IL-12/23p40 (red line), and IL-10 (black line). The means +/− SEM of 3 experiments are shown. (F–I) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with LPS for 4 hrs. Il-10 (F), Arg1 (G), Il-33 (H), and Hmox-1 (I) mRNA levels were determined by qPCR. The means +/−SEM of at least 3 independent experiments are shown. (J) WT (black bars) or STAT1 −/− BMDMs (striped bars) were left unprimed or primed with IFN-γ then stimulated with LPS. TNFα (left) and IL-12/23p40 (right) were measured in the supernatants 8 hours after stimulation. Protein was measured by ELISA. The means +/− SD of triplicates are shown.

    Techniques Used: Activation Assay, Enzyme-linked Immunosorbent Assay, Real-time Polymerase Chain Reaction

    20) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    21) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    22) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    23) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    24) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    25) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    26) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    27) Product Images from "ICP0 antagonizes Stat 1-dependent repression of herpes simplex virus: implications for the regulation of viral latency"

    Article Title: ICP0 antagonizes Stat 1-dependent repression of herpes simplex virus: implications for the regulation of viral latency

    Journal: Virology Journal

    doi: 10.1186/1743-422X-3-44

    Replication of ICP0 - and ICP4 - viruses in cell culture and immunodeficient mice . Vero cells were A . untreated or B . treated with 200 U per ml of IFN-β and were inoculated with 2.5 pfu per cell of wild-type HSV-1 (KOS), an ICP0 - virus (0 - -GFP), or an ICP4 - virus (n12). The mean ± sem of the logarithm of viral titers recovered from Vero cells is plotted over time (n = 4 per time point). C . Rag2 -/- stat1 -/- mice and D . rag2 -/- mice were inoculated with 2 × 10 5 pfu per eye of the ICP0 - virus 0 - -GFP or the ICP4 - virus n12 (n = 4 mice per group). The mean ± sem of the logarithm of viral titers recovered from mouse eyes is plotted over time (open black symbols). Dashed lines indicate the lower limit of detection of each plaque assay. The survival of 0 - -GFP-infected mice and ICP4 - virus-infected mice is plotted over time (open red symbols).
    Figure Legend Snippet: Replication of ICP0 - and ICP4 - viruses in cell culture and immunodeficient mice . Vero cells were A . untreated or B . treated with 200 U per ml of IFN-β and were inoculated with 2.5 pfu per cell of wild-type HSV-1 (KOS), an ICP0 - virus (0 - -GFP), or an ICP4 - virus (n12). The mean ± sem of the logarithm of viral titers recovered from Vero cells is plotted over time (n = 4 per time point). C . Rag2 -/- stat1 -/- mice and D . rag2 -/- mice were inoculated with 2 × 10 5 pfu per eye of the ICP0 - virus 0 - -GFP or the ICP4 - virus n12 (n = 4 mice per group). The mean ± sem of the logarithm of viral titers recovered from mouse eyes is plotted over time (open black symbols). Dashed lines indicate the lower limit of detection of each plaque assay. The survival of 0 - -GFP-infected mice and ICP4 - virus-infected mice is plotted over time (open red symbols).

    Techniques Used: Cell Culture, Mouse Assay, Plaque Assay, Infection

    Measurement of KOS and 0 - -GFP viral genome loads in the trigeminal ganglia of HSV-1 latently infected mice . A . Dotblot of HSV-1 VP16 PCR products. Each
    Figure Legend Snippet: Measurement of KOS and 0 - -GFP viral genome loads in the trigeminal ganglia of HSV-1 latently infected mice . A . Dotblot of HSV-1 VP16 PCR products. Each "dot" contains VP16 PCR product amplified from the TG DNA of a single mouse, and the n-values indicate numbers of mice per group. TG harvested from uninfected (UI) mice served as negative controls for the PCR. TG harvested from mice dying of encephalitis (Day 9 p.i.) belonged to one of the following groups: rag2 -/- ifnar -/- mice, ifnar -/- ifngr -/- mice, or stat1 -/- mice inoculated with 2 × 10 4 pfu per eye of 0 - -GFP. TG harvested from mice that were latently infected with HSV-1 (Day 40 p.i.) belonged to one of the following groups: strain 129 mice inoculated with 2 × 10 5 pfu per eye of KOS; strain 129 mice, ifngr -/- mice, or ifnar -/- mice inoculated with 2 × 10 5 pfu per eye of 0 - -GFP; or stat1 -/- mice inoculated with 2 × 10 4 pfu per eye of 0 - -GFP. The standard curve on the right consists of PCR products amplified from a two-fold dilution series of VP16 plasmid DNA. B . The ratio of yields of VP16 to competitor PCR product yields (competitor dotblot not shown) was used to estimate viral genome copy number per PCR. The logarithm of viral genomes per TG , y, was plotted as a function of the mean logarithm of the ratio of VP16 PCR product yield: competitor PCR product yield , x, amplified from duplicate PCRs of each dilution of VP16 plasmid (error bars indicate the standard deviation between duplicate PCRs). The relationship between viral genome load and PCR product yields was described by the equation, y = 0.2556•x 3 + 0.1055•x 2 + 1.2079•x + 5.9309 (r 2 = 0.99). The number of HSV-1 genomes per TG in each sample was derived from fitting the data shown in panel A to the standard curve shown in panel B. C . Number of HSV-1 genomes per TG in mice that were uninfected or were latently infected with KOS or 0 - -GFP. The dashed line indicates the lower limit of detection of the PCR assay. Asterisks denote significant differences in viral genome load per TG relative to strain 129 mice latently infected with KOS (p

    Techniques Used: Infection, Mouse Assay, Polymerase Chain Reaction, Amplification, Plasmid Preparation, Standard Deviation, Derivative Assay

    Loss of IFN-α/β receptors or Stat 1 impairs an innate host response that represses KOS-GFP and 0 - -GFP at the site of inoculation . Mice were inoculated with 2 × 10 5 pfu per eye of A . HSV-1 strain KOS-GFP, or B . the ICP0 - virus, 0 - -GFP. GFP fluorescence was recorded in the right eyes of strain 129 mice, rag2 -/- mice (lymphocyte-deficient), ifngr -/- mice (IFN-γ receptor-null), ifnar -/- mice (IFN-α/β receptor-null), ifnar -/- ifngr -/- mice, stat1 -/- mice, rag2 -/- stat1 -/- mice, and rag2 -/- ifnar -/- mice. Representative photographs are shown of GFP fluorescence in the virus-infected eye of one mouse per group photographed over time at 36, 60, and 84 hours p.i. (4× magnification; 39 ms exposure for KOS-GFP; 63 ms exposure for 0 - -GFP).
    Figure Legend Snippet: Loss of IFN-α/β receptors or Stat 1 impairs an innate host response that represses KOS-GFP and 0 - -GFP at the site of inoculation . Mice were inoculated with 2 × 10 5 pfu per eye of A . HSV-1 strain KOS-GFP, or B . the ICP0 - virus, 0 - -GFP. GFP fluorescence was recorded in the right eyes of strain 129 mice, rag2 -/- mice (lymphocyte-deficient), ifngr -/- mice (IFN-γ receptor-null), ifnar -/- mice (IFN-α/β receptor-null), ifnar -/- ifngr -/- mice, stat1 -/- mice, rag2 -/- stat1 -/- mice, and rag2 -/- ifnar -/- mice. Representative photographs are shown of GFP fluorescence in the virus-infected eye of one mouse per group photographed over time at 36, 60, and 84 hours p.i. (4× magnification; 39 ms exposure for KOS-GFP; 63 ms exposure for 0 - -GFP).

    Techniques Used: Mouse Assay, Fluorescence, Infection, Mass Spectrometry

    Loss of Stat 1 alleviates innate host repression of ICP0 - viruses in vivo . A . Strain 129 mice, rag2 -/- mice, PML -/- mice, or stat1 -/- mice were inoculated with 2 × 10 5 pfu per eye of the ICP0 - virus n212 (n = 4 mice per group). The mean ± sem of the logarithm of viral titers recovered from mouse eyes is plotted over time. B . Strain 129 mice, rag2 -/- mice, stat1 -/- mice, or rag2 -/- stat1 -/- mice were inoculated with 2 × 10 5 pfu per eye of the ICP0 - virus, 0 - -GFP (n = 4 mice per group). Dashed lines indicate the lower limit of detection of the plaque assay. C . Survival of strain 129 mice, rag2 -/- mice, PML -/- mice, stat1 -/- mice, or rag2 -/- stat1 -/- mice infected with the ICP0 - viruses, n212 or 0 - -GFP. Bars represent the mean ± sem of survival frequency of ICP0 - virus-infected mice at day 60 p.i. (n = 3 experiments; Σn = 14 mice per group).
    Figure Legend Snippet: Loss of Stat 1 alleviates innate host repression of ICP0 - viruses in vivo . A . Strain 129 mice, rag2 -/- mice, PML -/- mice, or stat1 -/- mice were inoculated with 2 × 10 5 pfu per eye of the ICP0 - virus n212 (n = 4 mice per group). The mean ± sem of the logarithm of viral titers recovered from mouse eyes is plotted over time. B . Strain 129 mice, rag2 -/- mice, stat1 -/- mice, or rag2 -/- stat1 -/- mice were inoculated with 2 × 10 5 pfu per eye of the ICP0 - virus, 0 - -GFP (n = 4 mice per group). Dashed lines indicate the lower limit of detection of the plaque assay. C . Survival of strain 129 mice, rag2 -/- mice, PML -/- mice, stat1 -/- mice, or rag2 -/- stat1 -/- mice infected with the ICP0 - viruses, n212 or 0 - -GFP. Bars represent the mean ± sem of survival frequency of ICP0 - virus-infected mice at day 60 p.i. (n = 3 experiments; Σn = 14 mice per group).

    Techniques Used: In Vivo, Mouse Assay, Plaque Assay, Infection

    A Stat1-dependent host response restricts the spread of HSV-1 strain KOS-GFP into the central nervous system . Strain 129 mice, rag2 -/- mice, stat1 -/- mice, or rag2 -/- stat1 -/- mice were inoculated with 2 × 10 5 pfu per eye of HSV-1 strain KOS-GFP. A . The mean ± sem of the logarithm of viral titers recovered from homogenates of mouse eyes, TG, and hindbrain is plotted as a function of the time p.i. at which tissues were harvested (n = 5 per time point). Asterisks denote significant differences between stat1 +/+ versus stat1 -/- tissues (p
    Figure Legend Snippet: A Stat1-dependent host response restricts the spread of HSV-1 strain KOS-GFP into the central nervous system . Strain 129 mice, rag2 -/- mice, stat1 -/- mice, or rag2 -/- stat1 -/- mice were inoculated with 2 × 10 5 pfu per eye of HSV-1 strain KOS-GFP. A . The mean ± sem of the logarithm of viral titers recovered from homogenates of mouse eyes, TG, and hindbrain is plotted as a function of the time p.i. at which tissues were harvested (n = 5 per time point). Asterisks denote significant differences between stat1 +/+ versus stat1 -/- tissues (p

    Techniques Used: Mouse Assay

    28) Product Images from "IFN-γ prevents adenosine receptor (A2bR) upregulation to sustain the macrophage activation response"

    Article Title: IFN-γ prevents adenosine receptor (A2bR) upregulation to sustain the macrophage activation response

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1501139

    IFN-γ preferentially inhibits LPS-induced A2bR expression in macrophages (A) mRNA expression of A1r (dotted bars), A2ar (horizontally striped bars), A2br (diagonally striped bars), and A3r (solid black bars) in unprimed and IFN-γ primed BMDMs stimulated for 4 hours. The means +/− SEM of 3 independent experiments are shown. (B,D) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with the indicated TLR agonists for 4 hours. A2bR (B) and A2aR (D) mRNA levels were determined by qPCR. The means +/−SEM of at least 3 independent determinations are shown. (C) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with LPS over time. A2bR mRNA levels were determined by qPCR. The means +/−SEM of 2 independent experiments are shown. (D) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with the indicated TLR agonists for 4hrs. A2aR mRNA levels were determined by qPCR. The means +/−SEM of at least 3 independent determinations are shown. (E) WT BMDMs (black bars) or STAT1 −/− BMDMs (striped bars) were left unprimed or IFN-γ primed, then stimulated with LPS for 4 hours. A2bR mRNA levels were determined by qPCR. The mean +/−SEM of at least 3 independent determinations are shown.
    Figure Legend Snippet: IFN-γ preferentially inhibits LPS-induced A2bR expression in macrophages (A) mRNA expression of A1r (dotted bars), A2ar (horizontally striped bars), A2br (diagonally striped bars), and A3r (solid black bars) in unprimed and IFN-γ primed BMDMs stimulated for 4 hours. The means +/− SEM of 3 independent experiments are shown. (B,D) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with the indicated TLR agonists for 4 hours. A2bR (B) and A2aR (D) mRNA levels were determined by qPCR. The means +/−SEM of at least 3 independent determinations are shown. (C) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with LPS over time. A2bR mRNA levels were determined by qPCR. The means +/−SEM of 2 independent experiments are shown. (D) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with the indicated TLR agonists for 4hrs. A2aR mRNA levels were determined by qPCR. The means +/−SEM of at least 3 independent determinations are shown. (E) WT BMDMs (black bars) or STAT1 −/− BMDMs (striped bars) were left unprimed or IFN-γ primed, then stimulated with LPS for 4 hours. A2bR mRNA levels were determined by qPCR. The mean +/−SEM of at least 3 independent determinations are shown.

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction

    IFN-γ prolongs the macrophage activation state (A,C) Cytokine production by LPS stimulated unprimed (black squares, solid line) or IFN- γ primed (gray circles, solid line) BMDMs over time. TNFα (A) and IL-12/23p40 (C) was detected by ELISA. The means +/− SEM of 3 independent experiments are shown. (B,D) Unprimed (black squares, solid line) or IFN- γ primed (gray circles, solid line) BMDMs were stimulated with LPS then washed with PBS (break in y-axis) and replaced with LPS-free media and monitored over the next 1–6 hours for TNFα (B), IL-12/23p40 (D). (E) BMDMs were stimulated with LPS alone or in the presence of increasing doses of POM-1. 8 hours post stimulation, cytokine production was assessed by ELISA for TNFα (blue line), IL-12/23p40 (red line), and IL-10 (black line). The means +/− SEM of 3 experiments are shown. (F–I) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with LPS for 4 hrs. Il-10 (F), Arg1 (G), Il-33 (H), and Hmox-1 (I) mRNA levels were determined by qPCR. The means +/−SEM of at least 3 independent experiments are shown. (J) WT (black bars) or STAT1 −/− BMDMs (striped bars) were left unprimed or primed with IFN-γ then stimulated with LPS. TNFα (left) and IL-12/23p40 (right) were measured in the supernatants 8 hours after stimulation. Protein was measured by ELISA. The means +/− SD of triplicates are shown.
    Figure Legend Snippet: IFN-γ prolongs the macrophage activation state (A,C) Cytokine production by LPS stimulated unprimed (black squares, solid line) or IFN- γ primed (gray circles, solid line) BMDMs over time. TNFα (A) and IL-12/23p40 (C) was detected by ELISA. The means +/− SEM of 3 independent experiments are shown. (B,D) Unprimed (black squares, solid line) or IFN- γ primed (gray circles, solid line) BMDMs were stimulated with LPS then washed with PBS (break in y-axis) and replaced with LPS-free media and monitored over the next 1–6 hours for TNFα (B), IL-12/23p40 (D). (E) BMDMs were stimulated with LPS alone or in the presence of increasing doses of POM-1. 8 hours post stimulation, cytokine production was assessed by ELISA for TNFα (blue line), IL-12/23p40 (red line), and IL-10 (black line). The means +/− SEM of 3 experiments are shown. (F–I) Unprimed BMDMs (black bars) and IFN-γ primed BMDMs (gray bars) were stimulated with LPS for 4 hrs. Il-10 (F), Arg1 (G), Il-33 (H), and Hmox-1 (I) mRNA levels were determined by qPCR. The means +/−SEM of at least 3 independent experiments are shown. (J) WT (black bars) or STAT1 −/− BMDMs (striped bars) were left unprimed or primed with IFN-γ then stimulated with LPS. TNFα (left) and IL-12/23p40 (right) were measured in the supernatants 8 hours after stimulation. Protein was measured by ELISA. The means +/− SD of triplicates are shown.

    Techniques Used: Activation Assay, Enzyme-linked Immunosorbent Assay, Real-time Polymerase Chain Reaction

    29) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    30) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    31) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    32) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    33) Product Images from "Type I Interferon Induced Epigenetic Regulation of Macrophages Suppresses Innate and Adaptive Immunity in Acute Respiratory Viral Infection"

    Article Title: Type I Interferon Induced Epigenetic Regulation of Macrophages Suppresses Innate and Adaptive Immunity in Acute Respiratory Viral Infection

    Journal: PLoS Pathogens

    doi: 10.1371/journal.ppat.1005338

    Setdb2 expression by Mϕ is dependent on JAK-STAT pathway and IRF7. (A-C) RT-PCR of Setdb2 in BM-Mϕ (A, B) and CD11b + cells (C) from IAV-infected lungs. (A) Untreated and IFN-I-stimulated BM-Mϕ were treated with a vehicle control or the JAK inhibitor tofacitinib at the time of stimulation. (B) Control and Stat1 -/- BM-Mϕ were stimulated with media or IFN-I for 5 hours. (A, B) Data are mean ± SEM relative to unstimulated cells; n = 3 independent experiments. (C) CD11b + cells were isolated from the lungs of control and Stat1 -/- mice inoculated with IAV (1 x 10 4 PFU). Data are mean ± SEM relative to control cells on day 4 post-infection; n = 8–12 mice. (D, E) RT-PCR of Irf3 (D) and Irf7 (E) in control BM-Mϕ stimulated with IFN-I for the indicated time course. Data are mean ± SEM relative to unstimulated cells; n = 2–3 independent experiments (F, G) RT-PCR of Setdb2 and Irf3 / Irf7 in BM-Mϕ treated with control, IRF3, or IRF7 siRNA and stimulated with IFN-I for 24 hours. Data are mean ± SEM relative to cells treated with control siRNA; n = 3 independent experiments. (H, I) ChIP analysis of STAT1 (H) and IRF7 (I) binding in the Setdb2 promoter in control and IFN-I-stimulated BM- Mϕ after 24 hours. Data are mean ± SEM relative to IgG control; n = 2–3 independent experiments. N.D.; not detected. * p
    Figure Legend Snippet: Setdb2 expression by Mϕ is dependent on JAK-STAT pathway and IRF7. (A-C) RT-PCR of Setdb2 in BM-Mϕ (A, B) and CD11b + cells (C) from IAV-infected lungs. (A) Untreated and IFN-I-stimulated BM-Mϕ were treated with a vehicle control or the JAK inhibitor tofacitinib at the time of stimulation. (B) Control and Stat1 -/- BM-Mϕ were stimulated with media or IFN-I for 5 hours. (A, B) Data are mean ± SEM relative to unstimulated cells; n = 3 independent experiments. (C) CD11b + cells were isolated from the lungs of control and Stat1 -/- mice inoculated with IAV (1 x 10 4 PFU). Data are mean ± SEM relative to control cells on day 4 post-infection; n = 8–12 mice. (D, E) RT-PCR of Irf3 (D) and Irf7 (E) in control BM-Mϕ stimulated with IFN-I for the indicated time course. Data are mean ± SEM relative to unstimulated cells; n = 2–3 independent experiments (F, G) RT-PCR of Setdb2 and Irf3 / Irf7 in BM-Mϕ treated with control, IRF3, or IRF7 siRNA and stimulated with IFN-I for 24 hours. Data are mean ± SEM relative to cells treated with control siRNA; n = 3 independent experiments. (H, I) ChIP analysis of STAT1 (H) and IRF7 (I) binding in the Setdb2 promoter in control and IFN-I-stimulated BM- Mϕ after 24 hours. Data are mean ± SEM relative to IgG control; n = 2–3 independent experiments. N.D.; not detected. * p

    Techniques Used: Expressing, Reverse Transcription Polymerase Chain Reaction, Infection, Isolation, Mouse Assay, Chromatin Immunoprecipitation, Binding Assay

    Setdb2 suppresses the expression of antiviral genes and cytokine production nu BM-Mϕ. Gene expression (A, C) and cytokine production (B) by control and Setdb2 -/- BM-Mϕ stimulated with IFN-I for 24 hours. Data represents the mean ± SEM of 3 independent experiments. (A) Comparison of antiviral and proinflammatory genes by RT-PCR. Values on scatter plot represent log 10 (Δ Ct ). The gray lines represent a 2-fold change in gene expression; upregulated genes (red dots), downregulated genes (green dots). (B) Concentration of IL-1β, IL-6, IL-10, IL-12p40, G-GSF, and TNF-α in the supernatants of control and Setdb2 -/- BM-Mϕ. (C) RT-PCR of Isg15 and Mx1 . Data were normalized to control BM-Mϕ. (D-G) Control and Setdb2 -/- BM-Mϕ were treated with a vehicle control, IFN-I (D-G) , or IFN-II (F, G) for 24 hours. Data are mean ± SEM relative to IgG control; n = 2–3 experiments (D, E) ChIP analysis of Setdb2 binding and H3K9 tri-methylation in the Isg15 (D) and Mx1 (E) promoter. (F, G) ChIP analysis of STAT1 (F) and IRF7 (G) binding in the Mx1 promoter. (H) Control and Setdb2 ff Lyz2 cre+ mice inoculated with a sublethal dose of IAV (1 x 10 4 PFU). ) RT-PCR of Rnasel , Pkr , Mx1 , and Isg15 in infected lungs on day 4 post-infection. Data are mean ± SEM (n = 6–14 mice) from 2–3 independent experiments. * p
    Figure Legend Snippet: Setdb2 suppresses the expression of antiviral genes and cytokine production nu BM-Mϕ. Gene expression (A, C) and cytokine production (B) by control and Setdb2 -/- BM-Mϕ stimulated with IFN-I for 24 hours. Data represents the mean ± SEM of 3 independent experiments. (A) Comparison of antiviral and proinflammatory genes by RT-PCR. Values on scatter plot represent log 10 (Δ Ct ). The gray lines represent a 2-fold change in gene expression; upregulated genes (red dots), downregulated genes (green dots). (B) Concentration of IL-1β, IL-6, IL-10, IL-12p40, G-GSF, and TNF-α in the supernatants of control and Setdb2 -/- BM-Mϕ. (C) RT-PCR of Isg15 and Mx1 . Data were normalized to control BM-Mϕ. (D-G) Control and Setdb2 -/- BM-Mϕ were treated with a vehicle control, IFN-I (D-G) , or IFN-II (F, G) for 24 hours. Data are mean ± SEM relative to IgG control; n = 2–3 experiments (D, E) ChIP analysis of Setdb2 binding and H3K9 tri-methylation in the Isg15 (D) and Mx1 (E) promoter. (F, G) ChIP analysis of STAT1 (F) and IRF7 (G) binding in the Mx1 promoter. (H) Control and Setdb2 ff Lyz2 cre+ mice inoculated with a sublethal dose of IAV (1 x 10 4 PFU). ) RT-PCR of Rnasel , Pkr , Mx1 , and Isg15 in infected lungs on day 4 post-infection. Data are mean ± SEM (n = 6–14 mice) from 2–3 independent experiments. * p

    Techniques Used: Expressing, Reverse Transcription Polymerase Chain Reaction, Concentration Assay, Chromatin Immunoprecipitation, Binding Assay, Methylation, Mouse Assay, Infection

    34) Product Images from "Re-evaluating the role of natural killer cells in innate resistance to herpes simplex virus type 1"

    Article Title: Re-evaluating the role of natural killer cells in innate resistance to herpes simplex virus type 1

    Journal: Virology Journal

    doi: 10.1186/1743-422X-2-56

    Effect of Stat 1 on innate resistance to HSV-1 . Wild-type (strain 129) mice, rag2 -/- mice, stat1 -/- mice, and rag2 -/- stat1 -/- mice were inoculated with 2 × 10 5 pfu/eye of HSV-1 strain KOS-GFP. A. Eyes of KOS-GFP-infected mice on days 1, 2, 3, and 4 p.i (4× magnification, illuminated with 360–400 nm light which excites GFP). A representative mouse from each group was sequentially imaged on days 1 through 4 p.i. B. Replication of HSV-1 strain KOS-GFP in the eyes of mice (mean ± SEM; n= 6; dashed line denotes lower limit of detection). Asterisks denote times at which stat1 -/- mice shed more virus than stat1 +/+ mice (p
    Figure Legend Snippet: Effect of Stat 1 on innate resistance to HSV-1 . Wild-type (strain 129) mice, rag2 -/- mice, stat1 -/- mice, and rag2 -/- stat1 -/- mice were inoculated with 2 × 10 5 pfu/eye of HSV-1 strain KOS-GFP. A. Eyes of KOS-GFP-infected mice on days 1, 2, 3, and 4 p.i (4× magnification, illuminated with 360–400 nm light which excites GFP). A representative mouse from each group was sequentially imaged on days 1 through 4 p.i. B. Replication of HSV-1 strain KOS-GFP in the eyes of mice (mean ± SEM; n= 6; dashed line denotes lower limit of detection). Asterisks denote times at which stat1 -/- mice shed more virus than stat1 +/+ mice (p

    Techniques Used: Mouse Assay, Infection

    35) Product Images from "Cutting Edge: The Th1 Response Inhibits the Generation of Peripheral Regulatory T Cells"

    Article Title: Cutting Edge: The Th1 Response Inhibits the Generation of Peripheral Regulatory T Cells

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.0903412

    STAT1 but not Tbet inhibits peripheral Treg generation. Naive CD4 + T cells from WT, Tbet −/− , or STAT1 −/− DO11.10 mice were sorted, cultured under Th1 conditions, and transferred to sOVARag −/− recipients.
    Figure Legend Snippet: STAT1 but not Tbet inhibits peripheral Treg generation. Naive CD4 + T cells from WT, Tbet −/− , or STAT1 −/− DO11.10 mice were sorted, cultured under Th1 conditions, and transferred to sOVARag −/− recipients.

    Techniques Used: Mouse Assay, Cell Culture

    36) Product Images from "Stat2 loss leads to cytokine-independent, cell-mediated lethality in LPS-induced sepsis"

    Article Title: Stat2 loss leads to cytokine-independent, cell-mediated lethality in LPS-induced sepsis

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    doi: 10.1073/pnas.1221652110

    LPS-induced mortality in mice lacking IFN signaling mediators and sepsis-induced tissue inflammation in Stat2 −/− mice. ( A ) Survival curves in WT, Tyk2 −/− , Ifnar1 −/− , Stat1 −/− , and Stat2 −/−
    Figure Legend Snippet: LPS-induced mortality in mice lacking IFN signaling mediators and sepsis-induced tissue inflammation in Stat2 −/− mice. ( A ) Survival curves in WT, Tyk2 −/− , Ifnar1 −/− , Stat1 −/− , and Stat2 −/−

    Techniques Used: Mouse Assay

    37) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    38) Product Images from "STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1"

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1001343

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X
    Figure Legend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Techniques Used: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p
    Figure Legend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Techniques Used: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p
    Figure Legend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Techniques Used: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.
    Figure Legend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Techniques Used: Polymerase Chain Reaction

    39) Product Images from "Activation Mechanisms of Natural Killer Cells during Influenza Virus Infection"

    Article Title: Activation Mechanisms of Natural Killer Cells during Influenza Virus Infection

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0051858

    STAT1, but not STAT4, is required for granzyme B induction by NK cells in response to flu infection. CD45.2 + splenocytes from 129/Sv WT and STAT1 −/− (A) or from BALB/c WT and STAT4 −/− (B) mice were combined with CD45.1 + B6 splenocytes in vitro, then infected with flu. NK cells (DX5 + CD3 − CD19 − ) were analyzed for expression levels of IFN-γ (left panels) and granzyme B (right panels). Bar graphs represent the mean differences in percentage of IFN-γ + or granzyme B + CD45.2 + NK cells from infected samples over uninfected controls. Error bars represent the SEM of triplicate samples. Data are representative of four independent experiments. **, P
    Figure Legend Snippet: STAT1, but not STAT4, is required for granzyme B induction by NK cells in response to flu infection. CD45.2 + splenocytes from 129/Sv WT and STAT1 −/− (A) or from BALB/c WT and STAT4 −/− (B) mice were combined with CD45.1 + B6 splenocytes in vitro, then infected with flu. NK cells (DX5 + CD3 − CD19 − ) were analyzed for expression levels of IFN-γ (left panels) and granzyme B (right panels). Bar graphs represent the mean differences in percentage of IFN-γ + or granzyme B + CD45.2 + NK cells from infected samples over uninfected controls. Error bars represent the SEM of triplicate samples. Data are representative of four independent experiments. **, P

    Techniques Used: Infection, Mouse Assay, In Vitro, Expressing

    Activation of STAT1 in NK cells requires the direct action of type I IFNs during influenza infection. NK cells from infected (open histograms) and uninfected (shaded histograms) mice were analyzed for intracellular pSTAT1 following adoptive transfer (A) or co-culture (B). Adoptive transfer was as described in Figure 2 . For in vitro infection, CD45.2 + splenocytes from IFNAR +/− or IFNAR −/− mice were combined with CD45.1 + B6 splenocytes at 1∶1 ratio, then infected with flu. NK cells (NK1.1 + CD3 − ) from infected (open histograms) and uninfected (shaded histograms) samples were analyzed for intracellular pSTAT1. Values represent the percentages of pSTAT1 + NK cells. Data are representative of three independent experiments with 2–4 (A) or 1–3 (B) mice per group.
    Figure Legend Snippet: Activation of STAT1 in NK cells requires the direct action of type I IFNs during influenza infection. NK cells from infected (open histograms) and uninfected (shaded histograms) mice were analyzed for intracellular pSTAT1 following adoptive transfer (A) or co-culture (B). Adoptive transfer was as described in Figure 2 . For in vitro infection, CD45.2 + splenocytes from IFNAR +/− or IFNAR −/− mice were combined with CD45.1 + B6 splenocytes at 1∶1 ratio, then infected with flu. NK cells (NK1.1 + CD3 − ) from infected (open histograms) and uninfected (shaded histograms) samples were analyzed for intracellular pSTAT1. Values represent the percentages of pSTAT1 + NK cells. Data are representative of three independent experiments with 2–4 (A) or 1–3 (B) mice per group.

    Techniques Used: Activation Assay, Infection, Mouse Assay, Adoptive Transfer Assay, Co-Culture Assay, In Vitro

    40) Product Images from "Re-evaluating the role of natural killer cells in innate resistance to herpes simplex virus type 1"

    Article Title: Re-evaluating the role of natural killer cells in innate resistance to herpes simplex virus type 1

    Journal: Virology Journal

    doi: 10.1186/1743-422X-2-56

    Effect of Stat 1 on innate resistance to HSV-1 . Wild-type (strain 129) mice, rag2 -/- mice, stat1 -/- mice, and rag2 -/- stat1 -/- mice were inoculated with 2 × 10 5 pfu/eye of HSV-1 strain KOS-GFP. A. Eyes of KOS-GFP-infected mice on days 1, 2, 3, and 4 p.i (4× magnification, illuminated with 360–400 nm light which excites GFP). A representative mouse from each group was sequentially imaged on days 1 through 4 p.i. B. Replication of HSV-1 strain KOS-GFP in the eyes of mice (mean ± SEM; n= 6; dashed line denotes lower limit of detection). Asterisks denote times at which stat1 -/- mice shed more virus than stat1 +/+ mice (p
    Figure Legend Snippet: Effect of Stat 1 on innate resistance to HSV-1 . Wild-type (strain 129) mice, rag2 -/- mice, stat1 -/- mice, and rag2 -/- stat1 -/- mice were inoculated with 2 × 10 5 pfu/eye of HSV-1 strain KOS-GFP. A. Eyes of KOS-GFP-infected mice on days 1, 2, 3, and 4 p.i (4× magnification, illuminated with 360–400 nm light which excites GFP). A representative mouse from each group was sequentially imaged on days 1 through 4 p.i. B. Replication of HSV-1 strain KOS-GFP in the eyes of mice (mean ± SEM; n= 6; dashed line denotes lower limit of detection). Asterisks denote times at which stat1 -/- mice shed more virus than stat1 +/+ mice (p

    Techniques Used: Mouse Assay, Infection

    Related Articles

    Inhibition:

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1
    Article Snippet: .. It is also known that, unlike T-bet and STAT1, genetic ablation of both T-bet and Eomes results in a compound hyper-Th17 phenotype but, again, the increase in IL-17 production was mirrored by a corresponding reduction in Th1 responses, making it unclear whether the phenotype was due to direct effects or a lack of IFN-γ/STAT1-dependent inhibition ( ). .. Based on the data presented here, we propose that both are true, that T-bet and Eomes can each limit Th17 responses through at least two shared mechanisms, one involving STAT1, with IFN-γ as an intermediary, and the other completely STAT1-independent.

    Gene Knockout:

    Article Title: The NS2 Protein of Human Respiratory Syncytial Virus Suppresses the Cytotoxic T-Cell Response as a Consequence of Suppressing the Type I Interferon Response
    Article Snippet: .. Seven- to 12-week-old BALB/c mice (Charles River Laboratories, Wilmington, MA) were used in all experiments except for those shown in Fig. through , which employed 7- to 11-week-old STAT1 gene knockout (KO) mice on an inbred 129S6/SvEv background or the control 129S6 mice (Taconic, Germantown, NY). .. Construction of the recombinant wild-type (wt) HRSV and the viruses lacking the NS1 and/or NS2 gene was described earlier ( , , , ); apart from the presence or absence of the NS genes, these viruses have identical genome sequences.

    other:

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1
    Article Snippet: These latter findings establish that T-bet can suppress Th17 responses independently of STAT1 and that, in WT cells, STAT1 and T-bet-mediated pathways may cooperate in achieving this shared function.

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1
    Article Snippet: We found that, while each exhibited a hyper-Th17 phenotype relative to WT controls, IL-17 production was higher in T-bet−/− donors than in STAT1−/− counterparts ( & ).

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1
    Article Snippet: Taken together, these contradictory observations suggest epistasis, meaning that the loss of STAT1 affects cellular processes that, while not directly related to Th17 differentiation, impact the overall quality of T cell responses, thereby hindering production of Th17-type cytokines.

    Mouse Assay:

    Article Title:
    Article Snippet: .. STAT1-deficient and STAT6-deficient mice were purchased from Taconic (Hudson, NY) and The Jackson Laboratory (Bar Harbor, ME), respectively. ..

    Article Title: The NS2 Protein of Human Respiratory Syncytial Virus Suppresses the Cytotoxic T-Cell Response as a Consequence of Suppressing the Type I Interferon Response
    Article Snippet: .. Seven- to 12-week-old BALB/c mice (Charles River Laboratories, Wilmington, MA) were used in all experiments except for those shown in Fig. through , which employed 7- to 11-week-old STAT1 gene knockout (KO) mice on an inbred 129S6/SvEv background or the control 129S6 mice (Taconic, Germantown, NY). .. Construction of the recombinant wild-type (wt) HRSV and the viruses lacking the NS1 and/or NS2 gene was described earlier ( , , , ); apart from the presence or absence of the NS genes, these viruses have identical genome sequences.

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1
    Article Snippet: .. Together with previous studies , these data indicate that both T cell- and non-T cell-derived IFN-γ can limit Th17-type inflammation in lymphopenic mice. donor cells after 7 days. (B) Data are compiled from 3 experiments (see To better define the mechanism for IFN-γ-mediated suppression, we compared the ability of STAT1- and T-bet-deficient T cells to generate Th17 responses in sOva Rag2−/− hosts. .. We found that, while each exhibited a hyper-Th17 phenotype relative to WT controls, IL-17 production was higher in T-bet−/− donors than in STAT1−/− counterparts ( & ).

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    Taconic Biosciences homozygous stat1 ko mice
    Characterization of bat NS1 recombinant viruses in vitro . (A and B) Viral growth of r/NS1HL17, r/NS1HL18, and r/NS1PR8 in MDCK (canine), A549 (human), and A549 <t>STAT1</t> −/− (human) cells and in primary kidney bat cell lines from Sturnira lilium and Artibeus lituratus . Cells were infected at an MOI of 0.01, and the viral supernatant was titrated as the number of PFU per milliliter at the indicated time points postinfection (p.i.). Shown are the means and SDs from three biological replicates. ANOVA for multiple comparisons was used, and those that were statistically significant ( P ≤ 0.05) were compared in groups two by two and the Bonferroni correction was applied (***, P
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    Characterization of bat NS1 recombinant viruses in vitro . (A and B) Viral growth of r/NS1HL17, r/NS1HL18, and r/NS1PR8 in MDCK (canine), A549 (human), and A549 STAT1 −/− (human) cells and in primary kidney bat cell lines from Sturnira lilium and Artibeus lituratus . Cells were infected at an MOI of 0.01, and the viral supernatant was titrated as the number of PFU per milliliter at the indicated time points postinfection (p.i.). Shown are the means and SDs from three biological replicates. ANOVA for multiple comparisons was used, and those that were statistically significant ( P ≤ 0.05) were compared in groups two by two and the Bonferroni correction was applied (***, P

    Journal: Journal of Virology

    Article Title: Specific Mutations in the PB2 Protein of Influenza A Virus Compensate for the Lack of Efficient Interferon Antagonism of the NS1 Protein of Bat Influenza A-Like Viruses

    doi: 10.1128/JVI.02021-17

    Figure Lengend Snippet: Characterization of bat NS1 recombinant viruses in vitro . (A and B) Viral growth of r/NS1HL17, r/NS1HL18, and r/NS1PR8 in MDCK (canine), A549 (human), and A549 STAT1 −/− (human) cells and in primary kidney bat cell lines from Sturnira lilium and Artibeus lituratus . Cells were infected at an MOI of 0.01, and the viral supernatant was titrated as the number of PFU per milliliter at the indicated time points postinfection (p.i.). Shown are the means and SDs from three biological replicates. ANOVA for multiple comparisons was used, and those that were statistically significant ( P ≤ 0.05) were compared in groups two by two and the Bonferroni correction was applied (***, P

    Article Snippet: Specific-pathogen-free C57BL/6 and 129S6/SvEv mice were purchased from The Jackson Laboratory and Taconic Biosciences, respectively, while homozygous STAT1 KO mice on a 129/Sv mouse background (129S6/SvEv- Stat1tm1Rds ) were initially purchased from Taconic Biosciences ( ).

    Techniques: Recombinant, In Vitro, Infection

    Characterization of bat NS1 recombinant viruses in mice unable to respond to type I IFN because of disruption of the STAT1 gene. (A) Six- to 8-week-old 129S6/SvEv WT mice were infected intranasally with the indicated amount of viruses, and PBS was used for mock infection. Mean body weights and Kaplan-Meier curves are shown ( n = 5 mice/group). Error bars represent SDs. The Mantel-Cox test was used to compare survival (**, P

    Journal: Journal of Virology

    Article Title: Specific Mutations in the PB2 Protein of Influenza A Virus Compensate for the Lack of Efficient Interferon Antagonism of the NS1 Protein of Bat Influenza A-Like Viruses

    doi: 10.1128/JVI.02021-17

    Figure Lengend Snippet: Characterization of bat NS1 recombinant viruses in mice unable to respond to type I IFN because of disruption of the STAT1 gene. (A) Six- to 8-week-old 129S6/SvEv WT mice were infected intranasally with the indicated amount of viruses, and PBS was used for mock infection. Mean body weights and Kaplan-Meier curves are shown ( n = 5 mice/group). Error bars represent SDs. The Mantel-Cox test was used to compare survival (**, P

    Article Snippet: Specific-pathogen-free C57BL/6 and 129S6/SvEv mice were purchased from The Jackson Laboratory and Taconic Biosciences, respectively, while homozygous STAT1 KO mice on a 129/Sv mouse background (129S6/SvEv- Stat1tm1Rds ) were initially purchased from Taconic Biosciences ( ).

    Techniques: Recombinant, Mouse Assay, Infection

    STAT1 does not display increased tyrosine phosphorylation nor does it translocate into nucleus of ToxB-treated CGNs. A , a 24-h time course of ToxB treatment (40 ng/ml) was performed in CGNs. Cell lysates were resolved by SDS-PAGE, and proteins were transferred to PVDF membranes. The blots were probed with antibodies against pSTAT1 (Tyr-701) and STAT1. Little to no increase in the tyrosine phosphorylation of STAT1 was observed in CGNs subjected to ToxB for up to 24 h. B , CGNs were incubated with control ( Con ) medium ± ToxB (40 ng/ml) for 8 h. Cells were fixed, and their nuclei were stained with DAPI. A primary antibody against pSTAT1 (Tyr-701) and a Cy3-conjugated secondary antibody were used to visualize pSTAT1. Incubation of CGNs with ToxB did not result in translocation of pSTAT1 into the nucleus. Scale bar , 10 μm.

    Journal: The Journal of Biological Chemistry

    Article Title: Signal Transducer and Activator of Transcription-5 Mediates Neuronal Apoptosis Induced by Inhibition of Rac GTPase Activity *

    doi: 10.1074/jbc.M111.302166

    Figure Lengend Snippet: STAT1 does not display increased tyrosine phosphorylation nor does it translocate into nucleus of ToxB-treated CGNs. A , a 24-h time course of ToxB treatment (40 ng/ml) was performed in CGNs. Cell lysates were resolved by SDS-PAGE, and proteins were transferred to PVDF membranes. The blots were probed with antibodies against pSTAT1 (Tyr-701) and STAT1. Little to no increase in the tyrosine phosphorylation of STAT1 was observed in CGNs subjected to ToxB for up to 24 h. B , CGNs were incubated with control ( Con ) medium ± ToxB (40 ng/ml) for 8 h. Cells were fixed, and their nuclei were stained with DAPI. A primary antibody against pSTAT1 (Tyr-701) and a Cy3-conjugated secondary antibody were used to visualize pSTAT1. Incubation of CGNs with ToxB did not result in translocation of pSTAT1 into the nucleus. Scale bar , 10 μm.

    Article Snippet: STAT1 KO mice and their wild-type littermates were obtained commercially from Taconic (Hudson, NY).

    Techniques: SDS Page, Incubation, Staining, Translocation Assay

    STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    doi: 10.4049/jimmunol.1001343

    Figure Lengend Snippet: STAT1-activating cytokines fail to suppress Th17 responses in the absence of STAT1 (A) CD4+ T cells were purified from WT, IFN-γ −/− , T-bet−/− and STAT1−/− mice. These were cultured under non-polarizing or Th17 conditions for 72 hours and shown is the percentage of cytokine + cells (CD4 + ). (B) Data are compiled from 3–5 experiments (Th17 conditions) and are presented as the Log2 fold change in cytokine + cells upon exposure to IFN-γ (Black Bars) or IL-27 (White Bars). Untreated groups have a relative value of 0 while cytokine-treated groups have values greater than or less than 0, depending on whether they have an enhancing (X > 0) or inhibitory effect (X

    Article Snippet: Together with previous studies , these data indicate that both T cell- and non-T cell-derived IFN-γ can limit Th17-type inflammation in lymphopenic mice. donor cells after 7 days. (B) Data are compiled from 3 experiments (see To better define the mechanism for IFN-γ-mediated suppression, we compared the ability of STAT1- and T-bet-deficient T cells to generate Th17 responses in sOva Rag2−/− hosts.

    Techniques: Purification, Mouse Assay, Cell Culture

    T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    doi: 10.4049/jimmunol.1001343

    Figure Lengend Snippet: T-bet and STAT1-deficient T cells exhibit a hyper-Th17 phenotype during systemic autoimmune disease (A) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11.10 mice and adoptively transferred into WT sOva Rag2−/− hosts. Shown is the percentage of cytokine + donor cells (CD4 + DO11.10 + ) on day 7 post-transfer. (B) Data are compiled from 3–5 experiments. One star denotes statistically significant differences between the indicated group and WT donors. Two stars denotes significant differences between the indicated group and T-bet−/− donors ( p

    Article Snippet: Together with previous studies , these data indicate that both T cell- and non-T cell-derived IFN-γ can limit Th17-type inflammation in lymphopenic mice. donor cells after 7 days. (B) Data are compiled from 3 experiments (see To better define the mechanism for IFN-γ-mediated suppression, we compared the ability of STAT1- and T-bet-deficient T cells to generate Th17 responses in sOva Rag2−/− hosts.

    Techniques: Purification, Mouse Assay

    Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    doi: 10.4049/jimmunol.1001343

    Figure Lengend Snippet: Phenotypic differences between T-bet- and STAT1-deficient donor T cells in sOva Rag2−/− mice (A) Naïve T cells were purified from either WT or IFN-γ −/− DO11.10 mice and then adoptively transferred into either WT or IFN-γ −/− sOva Rag2−/− hosts. At 7 days post-transfer, lymphocytes were stained directly ex vivo for flow cytometry. Shown are the percentages of total and activated donor T cells (CD4 + DO11.10 + ; CD25 + or CD44 high ). (B) Naïve T cells were purified from WT, T-bet−/− , STAT1−/− or T-bet−/− × STAT1−/− DO11 mice and transferred into sOva Rag2−/− hosts. Shown are the percentages of total and activated donor T cells after 7 days (A B) Data are compiled from 3 individual experiments. A star denotes statistically significant differences between the indicated group and WT controls ( p

    Article Snippet: Together with previous studies , these data indicate that both T cell- and non-T cell-derived IFN-γ can limit Th17-type inflammation in lymphopenic mice. donor cells after 7 days. (B) Data are compiled from 3 experiments (see To better define the mechanism for IFN-γ-mediated suppression, we compared the ability of STAT1- and T-bet-deficient T cells to generate Th17 responses in sOva Rag2−/− hosts.

    Techniques: Mouse Assay, Purification, Staining, Ex Vivo, Flow Cytometry, Cytometry

    Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: STAT1-activating cytokines limit Th17 responses through both T-bet-dependent and independent mechanisms 1

    doi: 10.4049/jimmunol.1001343

    Figure Lengend Snippet: Transcription of Th17-associated genes is influenced by both T-bet and STAT1-dependent pathways for additional PCR analysis.

    Article Snippet: Together with previous studies , these data indicate that both T cell- and non-T cell-derived IFN-γ can limit Th17-type inflammation in lymphopenic mice. donor cells after 7 days. (B) Data are compiled from 3 experiments (see To better define the mechanism for IFN-γ-mediated suppression, we compared the ability of STAT1- and T-bet-deficient T cells to generate Th17 responses in sOva Rag2−/− hosts.

    Techniques: Polymerase Chain Reaction