mouse il 17a  (Thermo Fisher)


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    IL 17A Mouse ELISA Kit
    Description:
    The mouse IL 17 ELISA is an enzyme linked immunosorbent assay for the quantitative detection of mouse IL 17 Mouse IL 17 mRNA is specifically expressed by activated alpha beta TCR CD2 CD8 T cells a small subset with a potentially important role in immune regulation IL 17 induces the secretion of IL 6 IL 8 PGE2 MCP 1 and G CSF by adherent cells like fibroblasts keratinocytes epithelial and endothelial cells IL 17 is also able to induce ICAM 1 surface expression of T cells IL 17 has been shown to support the growth of hemopoietic progenitors it has stimulatory effects on granulopoiesis in mice IL 17 may affect osteoclastic resorption and thereby mediate bone destruction accompanying some inflammatory diseases Astrocytes produce NO when stimulated by IL 17 which suggests a possible role for IL 17 in the inflammatory diseases of the CNS Forced expression of murine IL 17 induces immune responses and multiorgan inflammation Interleukin 17 is involved in the regulation of hematopoiesis and its effects are dependent on the physiological pathological status of the organism IL 17 expression in airways is upregulated upon allergen exposure like in allergic asthma Its crucial role in T cell activation suggests that IL 17 is involved in the development of autoimmune arthritis ConjugateBiotinSuitable Sample Typescell culture supernatant serumSample Volume50 µLReported ApplicationELISA
    Catalog Number:
    BMS6001
    Price:
    None
    Category:
    Kits and Assays
    Applications:
    Protein Assays and Analysis|Protein Biology
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    Structured Review

    Thermo Fisher mouse il 17a
    IHC analysis of the effect of BSYSC on <t>IL-17A</t> and FoxP3 protein expressions in the brain and spinal cord of mice. Note: ** p
    The mouse IL 17 ELISA is an enzyme linked immunosorbent assay for the quantitative detection of mouse IL 17 Mouse IL 17 mRNA is specifically expressed by activated alpha beta TCR CD2 CD8 T cells a small subset with a potentially important role in immune regulation IL 17 induces the secretion of IL 6 IL 8 PGE2 MCP 1 and G CSF by adherent cells like fibroblasts keratinocytes epithelial and endothelial cells IL 17 is also able to induce ICAM 1 surface expression of T cells IL 17 has been shown to support the growth of hemopoietic progenitors it has stimulatory effects on granulopoiesis in mice IL 17 may affect osteoclastic resorption and thereby mediate bone destruction accompanying some inflammatory diseases Astrocytes produce NO when stimulated by IL 17 which suggests a possible role for IL 17 in the inflammatory diseases of the CNS Forced expression of murine IL 17 induces immune responses and multiorgan inflammation Interleukin 17 is involved in the regulation of hematopoiesis and its effects are dependent on the physiological pathological status of the organism IL 17 expression in airways is upregulated upon allergen exposure like in allergic asthma Its crucial role in T cell activation suggests that IL 17 is involved in the development of autoimmune arthritis ConjugateBiotinSuitable Sample Typescell culture supernatant serumSample Volume50 µLReported ApplicationELISA
    https://www.bioz.com/result/mouse il 17a/product/Thermo Fisher
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    mouse il 17a - by Bioz Stars, 2021-06
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    Images

    1) Product Images from "Effects of Bu Shen Yi Sui Capsule on Th17/Treg cytokines in C57BL/6 mice with experimental autoimmune encephalomyelitis"

    Article Title: Effects of Bu Shen Yi Sui Capsule on Th17/Treg cytokines in C57BL/6 mice with experimental autoimmune encephalomyelitis

    Journal: BMC Complementary and Alternative Medicine

    doi: 10.1186/s12906-015-0572-0

    IHC analysis of the effect of BSYSC on IL-17A and FoxP3 protein expressions in the brain and spinal cord of mice. Note: ** p
    Figure Legend Snippet: IHC analysis of the effect of BSYSC on IL-17A and FoxP3 protein expressions in the brain and spinal cord of mice. Note: ** p

    Techniques Used: Immunohistochemistry, Mouse Assay

    qRT-PCR analysis of the effect of BSYSC on mRNA expressions of IL-17A and FoxP3 in the brain and spinal cord of mice. Note: * p
    Figure Legend Snippet: qRT-PCR analysis of the effect of BSYSC on mRNA expressions of IL-17A and FoxP3 in the brain and spinal cord of mice. Note: * p

    Techniques Used: Quantitative RT-PCR, Mouse Assay

    Western blot analysis of the effect of BSYSC on IL-17A and FoxP3 protein expressions in the brain and spinal cord of mice. (A) to (D) NC, EAE, EAE + PA and EAE + BSYSC mice. Note: * p
    Figure Legend Snippet: Western blot analysis of the effect of BSYSC on IL-17A and FoxP3 protein expressions in the brain and spinal cord of mice. (A) to (D) NC, EAE, EAE + PA and EAE + BSYSC mice. Note: * p

    Techniques Used: Western Blot, Mouse Assay

    ELISA analysis of IL-17A, IL-6, IL-23 and TGF-β1 expressions in the brain of the groups. Note: * p
    Figure Legend Snippet: ELISA analysis of IL-17A, IL-6, IL-23 and TGF-β1 expressions in the brain of the groups. Note: * p

    Techniques Used: Enzyme-linked Immunosorbent Assay

    2) Product Images from "Soluble IL-2R? (sCD25) Exacerbates Autoimmunity and Enhances the Development of Th17 Responses in Mice"

    Article Title: Soluble IL-2R? (sCD25) Exacerbates Autoimmunity and Enhances the Development of Th17 Responses in Mice

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0047748

    Exogenous sCD25 exacerbates autoimmunity. ( A ) MOG 33−55 immunized C57BL/6 mice developed clinical symptoms of EAE from day 12 after immunization with a peak of disease severity observed from day 19. Subcutaneous administration of recombinant sCD25 (25 µg/mouse) immediately prior to immunization and every 12 hours thereafter for 72 hrs resulted in a significant exacerbation in severity of symptoms during disease onset and induction. 6–7 mice used per group. ( B ) Mononuclear cells harvested from spinal cords of control (PBS) and sCD25 treated IL-17A-eGFP reporter mice (3 per group) on day 15 after immunization and analysed for expression of IL-17 and IFN-γ by CD4+ cells. ( C ) Cell numbers of CD4+IL-17+ and CD4+ IFNγ+ cells in spinal cords of IL-17A-eGFP reporter mice at day 15. Data representative of mean +/− std dev of 3 mice per group and 2 independent experiments.
    Figure Legend Snippet: Exogenous sCD25 exacerbates autoimmunity. ( A ) MOG 33−55 immunized C57BL/6 mice developed clinical symptoms of EAE from day 12 after immunization with a peak of disease severity observed from day 19. Subcutaneous administration of recombinant sCD25 (25 µg/mouse) immediately prior to immunization and every 12 hours thereafter for 72 hrs resulted in a significant exacerbation in severity of symptoms during disease onset and induction. 6–7 mice used per group. ( B ) Mononuclear cells harvested from spinal cords of control (PBS) and sCD25 treated IL-17A-eGFP reporter mice (3 per group) on day 15 after immunization and analysed for expression of IL-17 and IFN-γ by CD4+ cells. ( C ) Cell numbers of CD4+IL-17+ and CD4+ IFNγ+ cells in spinal cords of IL-17A-eGFP reporter mice at day 15. Data representative of mean +/− std dev of 3 mice per group and 2 independent experiments.

    Techniques Used: Mouse Assay, Recombinant, Expressing

    sCD25 acts early during Th17 development. Purified naive CD4+ T cells from IL-17AeGFP reporter mice activated under Th17 inducing conditions in the presence of sCD25 (20 µg/ml) or anti-IL-2 (10 µg/ml) for 48 hrs and examined for levels of ( A ) IL-17A and ( B ) RORγT expression by FACS. All data are representative of at least 3 independent experiments.
    Figure Legend Snippet: sCD25 acts early during Th17 development. Purified naive CD4+ T cells from IL-17AeGFP reporter mice activated under Th17 inducing conditions in the presence of sCD25 (20 µg/ml) or anti-IL-2 (10 µg/ml) for 48 hrs and examined for levels of ( A ) IL-17A and ( B ) RORγT expression by FACS. All data are representative of at least 3 independent experiments.

    Techniques Used: Purification, Mouse Assay, Expressing, FACS

    sCD25 enhances peripheral antigen specific Th17 responses. ( A ) Levels of IL-17A and IFNγ secreted by draining lymph node cells of mice immunized and treated as above (3 per group), isolated after 9 days, and restimulated ex vivo with MOG 33−55 (10 µg/ml) for 72 hours. ( B ) Percentage of CD4+ IL-17A-eGFP+ve cells after treatment as above and ex vivo restimulation for 72 hours. ( C ) Percentage and ( D ) relative number ratios of CD4+FoxP3+:CD4+FoxP3- T cells in the draining lymph nodes of both sCD25 and control treated immunized mice. 3 mice per group were analysed. Data in D G is representative of mean +/− standard deviation. Statistical Significance determined by unpaired student's t-test, * p≤0.05, **p≤0.01.
    Figure Legend Snippet: sCD25 enhances peripheral antigen specific Th17 responses. ( A ) Levels of IL-17A and IFNγ secreted by draining lymph node cells of mice immunized and treated as above (3 per group), isolated after 9 days, and restimulated ex vivo with MOG 33−55 (10 µg/ml) for 72 hours. ( B ) Percentage of CD4+ IL-17A-eGFP+ve cells after treatment as above and ex vivo restimulation for 72 hours. ( C ) Percentage and ( D ) relative number ratios of CD4+FoxP3+:CD4+FoxP3- T cells in the draining lymph nodes of both sCD25 and control treated immunized mice. 3 mice per group were analysed. Data in D G is representative of mean +/− standard deviation. Statistical Significance determined by unpaired student's t-test, * p≤0.05, **p≤0.01.

    Techniques Used: Mouse Assay, Isolation, Ex Vivo, Standard Deviation

    sCD25 enhances Th17 cell responses in vitro . ( A B ) Purified naive CD4+ T cells were activated under either Th17 or Th1 inducing conditions (as described in methods ) in the presence of a range of concentrations of sCD25 (20, 10, 5 or 1 µg/ml) or anti-IL-2 (10 µg/ml). Levels of IL-17A or IFNγ expression were determined after 96 hrs by ( A ) FACS and ( B ) ELISA. ( C ) Purified naive CD4+ T cells were activated under Treg inducing conditions, as described in methods , in the presence or absence of sCD25 (20µg/ml) and FoxP3 expression determined by FACS. ( D ) Naive CD4+ T cells were stained with CFSE (2.5 µM) prior to activation under Th17 conditions in presence or absence of sCD25 (20 µg/ml). After 96 hours, levels of intracellular IL-17A expression and CFSE dilution or 7AAD incorporation were determined by FACS. ( E ) Purified naive CD4+ T cells were activated under Th0, Th17 and Th17 sCD25 (20 µg/ml) conditions for 72 hours and levels of P-Stat3 (pY705) determined by FACS. All data are representative of 3 independent experiments. Statistical Significance determined by unpaired student's t-test, ∗ p≤0.05, **p≤0.01, ***p≤0.001.
    Figure Legend Snippet: sCD25 enhances Th17 cell responses in vitro . ( A B ) Purified naive CD4+ T cells were activated under either Th17 or Th1 inducing conditions (as described in methods ) in the presence of a range of concentrations of sCD25 (20, 10, 5 or 1 µg/ml) or anti-IL-2 (10 µg/ml). Levels of IL-17A or IFNγ expression were determined after 96 hrs by ( A ) FACS and ( B ) ELISA. ( C ) Purified naive CD4+ T cells were activated under Treg inducing conditions, as described in methods , in the presence or absence of sCD25 (20µg/ml) and FoxP3 expression determined by FACS. ( D ) Naive CD4+ T cells were stained with CFSE (2.5 µM) prior to activation under Th17 conditions in presence or absence of sCD25 (20 µg/ml). After 96 hours, levels of intracellular IL-17A expression and CFSE dilution or 7AAD incorporation were determined by FACS. ( E ) Purified naive CD4+ T cells were activated under Th0, Th17 and Th17 sCD25 (20 µg/ml) conditions for 72 hours and levels of P-Stat3 (pY705) determined by FACS. All data are representative of 3 independent experiments. Statistical Significance determined by unpaired student's t-test, ∗ p≤0.05, **p≤0.01, ***p≤0.001.

    Techniques Used: In Vitro, Purification, Expressing, FACS, Enzyme-linked Immunosorbent Assay, Staining, Activation Assay

    3) Product Images from "Blockage of P2X7 attenuates acute lung injury in mice by inhibiting NLRP3 inflammasome"

    Article Title: Blockage of P2X7 attenuates acute lung injury in mice by inhibiting NLRP3 inflammasome

    Journal: International Immunopharmacology

    doi: 10.1016/j.intimp.2015.04.035

    A438079 inhibits IFN-γ and IL-17A but not IL-10 production in lung tissues and BAL fluids. Cytokine level in tissue homogenate or BAL fluid was measured by ELISA. a and d, IFN-γ levels in lung tissues (a) and BAL fluid (d). b and e, IL-17A levels in lung tissues (b) and BAL fluid (e). c and f, IL-10 levels in lung tissues (c) and BAL fluid (f). Each bar represents mean ± SEM ( n = 6). ** P
    Figure Legend Snippet: A438079 inhibits IFN-γ and IL-17A but not IL-10 production in lung tissues and BAL fluids. Cytokine level in tissue homogenate or BAL fluid was measured by ELISA. a and d, IFN-γ levels in lung tissues (a) and BAL fluid (d). b and e, IL-17A levels in lung tissues (b) and BAL fluid (e). c and f, IL-10 levels in lung tissues (c) and BAL fluid (f). Each bar represents mean ± SEM ( n = 6). ** P

    Techniques Used: Enzyme-linked Immunosorbent Assay

    4) Product Images from "Blood coagulation factor XII drives adaptive immunity during neuroinflammation via CD87-mediated modulation of dendritic cells"

    Article Title: Blood coagulation factor XII drives adaptive immunity during neuroinflammation via CD87-mediated modulation of dendritic cells

    Journal: Nature Communications

    doi: 10.1038/ncomms11626

    Factor XII deficiency alters T-cell differentiation. ( a ) Tbx21 , Gata3 , Rorc and Foxp3 expression from LN cells at day 10 ( d 10 ) or d max as well as from brain-infiltrating leukocytes (BILs) at d max after MOG 35–55 immunization is determined by real-time reverse transcription–PCR using 18S rRNA for normalization. Data (mean±s.e.m. of five experiments) are given as fold change in normalized gene expression in animals relative to WT controls. ( b ) At d 10 after MOG 35–55 immunization, proliferation and cytokine production by CD4 + T cells purified from LN and restimulated with 10 μg ml −1 MOG 35–55 and irradiated (35 Gy) antigen-presenting cells in vitro for 48 h (upper panels), and by CD11c + DCs purified from spleens and incubated with 1 μg ml −1 LPS in vitro for 48 h (lower panels) are shown. ( c ) Mononuclear cells were isolated from the LN of WT and F12 −/− animals at d 10 post induction of EAE. Cells were polyclonal restimulated in vitro , stained with anti-CD3 and anti-CD4, fixed and permeabilized, stained intracellularly with anti-IL-17A and analysed by flow cytometry for the percentage of IL-17A-producing CD4 + T cells. ( d ) Cytokine production by purified BILs from MOG 35–55 -immunized WT or F12 −/− mice at d max after restimulation with 10 μg ml −1 MOG 35–55 for 48 h. ( e , f ) BILs and LNs were isolated from WT and F12 −/− animals at d max post induction of EAE and polyclonal restimulated in vitro . For the detection of the percentage of IL-17A-producing lymphocytes (CD45 high CD11b neg cells or CD4 + CD3 + T cells), BILs or LNs were stained with anti-CD11b and anti-CD45, or anti-CD3 and anti-CD4, fixed and permeabilized, stained intracellularly with anti-IL-17A and analysed by flow cytometry. In b – f , data are given as means±s.e.m. of three independent experiments, each performed in triplicate. For c , e and f , representative dot plots for IL-17A expression are shown. For a – f , non-parametric Mann–Whitney U -test. * P
    Figure Legend Snippet: Factor XII deficiency alters T-cell differentiation. ( a ) Tbx21 , Gata3 , Rorc and Foxp3 expression from LN cells at day 10 ( d 10 ) or d max as well as from brain-infiltrating leukocytes (BILs) at d max after MOG 35–55 immunization is determined by real-time reverse transcription–PCR using 18S rRNA for normalization. Data (mean±s.e.m. of five experiments) are given as fold change in normalized gene expression in animals relative to WT controls. ( b ) At d 10 after MOG 35–55 immunization, proliferation and cytokine production by CD4 + T cells purified from LN and restimulated with 10 μg ml −1 MOG 35–55 and irradiated (35 Gy) antigen-presenting cells in vitro for 48 h (upper panels), and by CD11c + DCs purified from spleens and incubated with 1 μg ml −1 LPS in vitro for 48 h (lower panels) are shown. ( c ) Mononuclear cells were isolated from the LN of WT and F12 −/− animals at d 10 post induction of EAE. Cells were polyclonal restimulated in vitro , stained with anti-CD3 and anti-CD4, fixed and permeabilized, stained intracellularly with anti-IL-17A and analysed by flow cytometry for the percentage of IL-17A-producing CD4 + T cells. ( d ) Cytokine production by purified BILs from MOG 35–55 -immunized WT or F12 −/− mice at d max after restimulation with 10 μg ml −1 MOG 35–55 for 48 h. ( e , f ) BILs and LNs were isolated from WT and F12 −/− animals at d max post induction of EAE and polyclonal restimulated in vitro . For the detection of the percentage of IL-17A-producing lymphocytes (CD45 high CD11b neg cells or CD4 + CD3 + T cells), BILs or LNs were stained with anti-CD11b and anti-CD45, or anti-CD3 and anti-CD4, fixed and permeabilized, stained intracellularly with anti-IL-17A and analysed by flow cytometry. In b – f , data are given as means±s.e.m. of three independent experiments, each performed in triplicate. For c , e and f , representative dot plots for IL-17A expression are shown. For a – f , non-parametric Mann–Whitney U -test. * P

    Techniques Used: Cell Differentiation, Expressing, Polymerase Chain Reaction, Purification, Irradiation, In Vitro, Incubation, Isolation, Staining, Flow Cytometry, Mouse Assay, MANN-WHITNEY

    FXII controls cytokine production via CD87. ( a ) Splenic cDCs from naive WT animals were stimulated with 1 μg ml −1 LPS in the absence and presence of 60 nM activated FXII (FXIIa). After 48 h, cytokine concentrations were measured in culture supernatants by ELISA. ( b ) Cytokine production of splenic cDCs from WT animals stimulated with 1 μg ml −1 LPS in the absence and presence of 60 nM non-cleavable FXII. After 48 h, cytokine concentrations were determined in culture supernatants by ELISA. ( c ) Cytokine production of splenic cDCs from CD87-deficient ( Cd87 −/− ) mice stimulated with 1 μg ml −1 LPS alone or in the absence and presence of 60 nM FXII for 48 h. ( d ) Cytokine production of splenic cDCs from CD11b-deficient ( Itgam −/− ) animals stimulated with 1 μg ml −1 LPS in the absence and presence of 60 nM FXII for 48 h. ( e ) Cytosolic cAMP formation measured in cDCs from WT or Cd87 −/− mice that were incubated with medium only (Ctrl) or stimulated with 1 μg ml −1 LPS for 10 min in the absence (Ctrl) or presence of 60 nM FXII. ( f ) Cytokine concentrations of IL-6 (left panel) and IL-23 (right panel) in the supernatants of WT cDCs stimulated with 1 μg ml −1 LPS or 60 nM FXII for 48 h in the presence of protein kinase A inhibitors (3 μM H-89 and 100 μM Rp-8-Br-cAMP). ( g ) Cytokine concentrations of IFN-γ, IL-17A, IL-6, IL-12 and IL-23 were measured in the supernatants from co-cultures of CD4 + T lymphocytes from WT (upper panel) or Cd87 −/− (lower panel) that were polyclonal activated together with cDCs from WT and Cd87 −/− in the absence or presence of 60 nM FXII. In a – g , data are given as means±s.e.m. of three independent experiments, each performed in duplicate (non-parametric Mann–Whitney U -test). * P
    Figure Legend Snippet: FXII controls cytokine production via CD87. ( a ) Splenic cDCs from naive WT animals were stimulated with 1 μg ml −1 LPS in the absence and presence of 60 nM activated FXII (FXIIa). After 48 h, cytokine concentrations were measured in culture supernatants by ELISA. ( b ) Cytokine production of splenic cDCs from WT animals stimulated with 1 μg ml −1 LPS in the absence and presence of 60 nM non-cleavable FXII. After 48 h, cytokine concentrations were determined in culture supernatants by ELISA. ( c ) Cytokine production of splenic cDCs from CD87-deficient ( Cd87 −/− ) mice stimulated with 1 μg ml −1 LPS alone or in the absence and presence of 60 nM FXII for 48 h. ( d ) Cytokine production of splenic cDCs from CD11b-deficient ( Itgam −/− ) animals stimulated with 1 μg ml −1 LPS in the absence and presence of 60 nM FXII for 48 h. ( e ) Cytosolic cAMP formation measured in cDCs from WT or Cd87 −/− mice that were incubated with medium only (Ctrl) or stimulated with 1 μg ml −1 LPS for 10 min in the absence (Ctrl) or presence of 60 nM FXII. ( f ) Cytokine concentrations of IL-6 (left panel) and IL-23 (right panel) in the supernatants of WT cDCs stimulated with 1 μg ml −1 LPS or 60 nM FXII for 48 h in the presence of protein kinase A inhibitors (3 μM H-89 and 100 μM Rp-8-Br-cAMP). ( g ) Cytokine concentrations of IFN-γ, IL-17A, IL-6, IL-12 and IL-23 were measured in the supernatants from co-cultures of CD4 + T lymphocytes from WT (upper panel) or Cd87 −/− (lower panel) that were polyclonal activated together with cDCs from WT and Cd87 −/− in the absence or presence of 60 nM FXII. In a – g , data are given as means±s.e.m. of three independent experiments, each performed in duplicate (non-parametric Mann–Whitney U -test). * P

    Techniques Used: Enzyme-linked Immunosorbent Assay, Mouse Assay, Incubation, MANN-WHITNEY

    FXII blockade protects from neuroinflammation and contact hypersensitivity. ( a ) Clinical scores of WT mice treated with rHA-Infestin-4 or vehicle starting on day 1 after EAE induction are shown. Representative data from two independent experiments are depicted ( Supplementary Table 3 ). ( b , c ) Histological analysis of spinal cord sections of WT and rHA-Infestin-4-treated mice at d max . Lumbar sections were stained with haematoxylin and eosin (HE) ( b ) to evaluate inflammatory foci or immunostained for Luxol fast blue (LFB) ( c ) to assess demyelination. Arrows indicate inflammation or demyelinated areas. Scale bars, 100 μm. ( d ) Cytokines produced by CD4 + T lymphocytes and DCs from WT mice treated with rHA-Infestin-4 or vehicle 10 days after immunization. Data from three independent experiments, each performed in duplicate are shown. Clinical scores of ( e ) MOG 35–55 -immunized WT mice and ( f ) proteolipid protein peptide 139–151-immunized SJL/JRj mice treated with rHA-Infestin-4 or vehicle starting at the first day of neurologic symptoms (arrow; for detailed information, see Supplementary Table 4 ). ( g ) Clinical, cumulative EAE scores and ( h ) disease incidence of Devic mice treated with rHA-Infestin or vehicle starting at postnatal day 20. ( i ) The motor coordination of Devic mice was assessed using the rotarod. The time t he mice remained on the rod was recorded. For each mouse, the average time of three trials followed by 30-min breaks was recorded daily. ( j ) Number of infiltrating CD4 + T cells within the central nervous system of Devic mice was analysed by flow cytometry at postnatal day 40. ( k ) Ear swelling of WT or F12 −/− mice following induction of contact hypersensitivity. Representative data from three independent experiments are shown. Quantification of 2,4-dinitrobenzenesulfonic acid sodium salt-induced proliferation, and IFN-γ and IL-17A production of LN cells from WT and F12 −/− mice. Representative data in quadruplicate wells from two independent experiments are shown. In a – j , 200 mg kg −1 body weight of rHA-Infestin-4 or vehicle was given once daily. In a – k , data are given as mean±s.e.m. * P
    Figure Legend Snippet: FXII blockade protects from neuroinflammation and contact hypersensitivity. ( a ) Clinical scores of WT mice treated with rHA-Infestin-4 or vehicle starting on day 1 after EAE induction are shown. Representative data from two independent experiments are depicted ( Supplementary Table 3 ). ( b , c ) Histological analysis of spinal cord sections of WT and rHA-Infestin-4-treated mice at d max . Lumbar sections were stained with haematoxylin and eosin (HE) ( b ) to evaluate inflammatory foci or immunostained for Luxol fast blue (LFB) ( c ) to assess demyelination. Arrows indicate inflammation or demyelinated areas. Scale bars, 100 μm. ( d ) Cytokines produced by CD4 + T lymphocytes and DCs from WT mice treated with rHA-Infestin-4 or vehicle 10 days after immunization. Data from three independent experiments, each performed in duplicate are shown. Clinical scores of ( e ) MOG 35–55 -immunized WT mice and ( f ) proteolipid protein peptide 139–151-immunized SJL/JRj mice treated with rHA-Infestin-4 or vehicle starting at the first day of neurologic symptoms (arrow; for detailed information, see Supplementary Table 4 ). ( g ) Clinical, cumulative EAE scores and ( h ) disease incidence of Devic mice treated with rHA-Infestin or vehicle starting at postnatal day 20. ( i ) The motor coordination of Devic mice was assessed using the rotarod. The time t he mice remained on the rod was recorded. For each mouse, the average time of three trials followed by 30-min breaks was recorded daily. ( j ) Number of infiltrating CD4 + T cells within the central nervous system of Devic mice was analysed by flow cytometry at postnatal day 40. ( k ) Ear swelling of WT or F12 −/− mice following induction of contact hypersensitivity. Representative data from three independent experiments are shown. Quantification of 2,4-dinitrobenzenesulfonic acid sodium salt-induced proliferation, and IFN-γ and IL-17A production of LN cells from WT and F12 −/− mice. Representative data in quadruplicate wells from two independent experiments are shown. In a – j , 200 mg kg −1 body weight of rHA-Infestin-4 or vehicle was given once daily. In a – k , data are given as mean±s.e.m. * P

    Techniques Used: Mouse Assay, Staining, Produced, Flow Cytometry

    5) Product Images from "Expression of Interleukin-17A in Lung Tissues of Irradiated Mice and the Influence of Dexamethasone"

    Article Title: Expression of Interleukin-17A in Lung Tissues of Irradiated Mice and the Influence of Dexamethasone

    Journal: The Scientific World Journal

    doi: 10.1155/2014/251067

    IL-17A expression in lung tissue detected by immunohistochemical method. It can be seen that cytoplasmic staining of RT group gradually deepened from the 1st week, peaked in the 4th week, declined in the 8th week, and reached a lower level in the 16th week but slightly higher than Sham group ( Table 1 , Figure 1 ). DXM application reduced mice IL-17A expression of RT group at indicated time points. The position of black arrows points to IL-17A-positive cells.
    Figure Legend Snippet: IL-17A expression in lung tissue detected by immunohistochemical method. It can be seen that cytoplasmic staining of RT group gradually deepened from the 1st week, peaked in the 4th week, declined in the 8th week, and reached a lower level in the 16th week but slightly higher than Sham group ( Table 1 , Figure 1 ). DXM application reduced mice IL-17A expression of RT group at indicated time points. The position of black arrows points to IL-17A-positive cells.

    Techniques Used: Expressing, Immunohistochemistry, Staining, Mouse Assay

    Expression of IL-17A in BALF at the indicated time points. The mice were sacrificed at the time of 1, 4, 8, and 16 weeks after irradiation, and BALF was collected for analysis of IL-17A contents. The contents of IL-17A in the BALF were analyzed by ELISA kits. Radiation stimulated an increase in the levels of IL-17A, but dexamethasone attenuated the IL-17A level in BALF. # P
    Figure Legend Snippet: Expression of IL-17A in BALF at the indicated time points. The mice were sacrificed at the time of 1, 4, 8, and 16 weeks after irradiation, and BALF was collected for analysis of IL-17A contents. The contents of IL-17A in the BALF were analyzed by ELISA kits. Radiation stimulated an increase in the levels of IL-17A, but dexamethasone attenuated the IL-17A level in BALF. # P

    Techniques Used: Expressing, Mouse Assay, Irradiation, Enzyme-linked Immunosorbent Assay

    6) Product Images from "The Aryl Hydrocarbon Receptor: Differential Contribution to T Helper 17 and T Cytotoxic 17 Cell Development"

    Article Title: The Aryl Hydrocarbon Receptor: Differential Contribution to T Helper 17 and T Cytotoxic 17 Cell Development

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0106955

    Cytokine mRNA and protein expression profiles of Th17 and Tc17 cells: effect of AhR modulation. Naïve CD4 + cells from AhR +/− (black bar) or AhR −/− mice (white bar) and naïve CD8 + cells from AhR +/− (grey bar) or AhR −/− mice (striped bar) were polarised under Th17/Tc17 conditions for 5 days in the presence of AhR antagonist (CH-223191) or AhR agonist (FICZ) both formulated in DMSO or with an equivalent amount of DMSO alone. Cells were harvested and total RNA prepared for the analysis of mRNA levels for IL-17A, IL-22, and IFN-γ using RT-PCR and the ΔΔ Ct method (A, C and E). Results were normalised against naive CD4 + or CD8 + cells and the housekeeping gene HPRT. Supernatants were also analysed for secreted cytokine by ELISA (B, D and F). Results are shown as mean ± SE for n = 3 independent experiments. Statistical significance of differences between DMSO control and AhR antagonist/agonist treated cells was analysed by one-way ANOVA. *, p
    Figure Legend Snippet: Cytokine mRNA and protein expression profiles of Th17 and Tc17 cells: effect of AhR modulation. Naïve CD4 + cells from AhR +/− (black bar) or AhR −/− mice (white bar) and naïve CD8 + cells from AhR +/− (grey bar) or AhR −/− mice (striped bar) were polarised under Th17/Tc17 conditions for 5 days in the presence of AhR antagonist (CH-223191) or AhR agonist (FICZ) both formulated in DMSO or with an equivalent amount of DMSO alone. Cells were harvested and total RNA prepared for the analysis of mRNA levels for IL-17A, IL-22, and IFN-γ using RT-PCR and the ΔΔ Ct method (A, C and E). Results were normalised against naive CD4 + or CD8 + cells and the housekeeping gene HPRT. Supernatants were also analysed for secreted cytokine by ELISA (B, D and F). Results are shown as mean ± SE for n = 3 independent experiments. Statistical significance of differences between DMSO control and AhR antagonist/agonist treated cells was analysed by one-way ANOVA. *, p

    Techniques Used: Expressing, Mouse Assay, Reverse Transcription Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

    The effect of AhR modulation on Th17 and Tc17 cell frequency. Naïve CD4 + cells from AhR +/− (A and E) or AhR −/− mice (B and F) and naïve CD8 + cells from AhR +/− (C and G) or AhR −/− mice (D and H) were polarised under Th17/Tc17 conditions for 5 days. Cells were then stimulated with PdBU and ionomycin in the presence of brefeldin A. The polarised cells were then permeabilised and stained using fluorescent anti-IL-17A (PE [Y-axis]) and -IFN-γ (APC [X-axis]) labelled antibodies. Cells (25000) were analysed by flow cytometry. The cells were cultured in the presence of AhR antagonist (CH-223191) (white bar) or AhR agonist (FICZ) (grey bar) both formulated in DMSO or with an equivalent amount of DMSO alone (black bar). Representative quadrant analyses are illustrated (A–D). The percentage of cells positive for IL-17, IL-17 and IFN-γ or IFN-γ alone was calculated by subtracting the isotype controls from the positive cells in each quadrant and are illustrated as % positive cells (E-H; mean ± SE; n = 3 independent experiments). Statistical significance of differences between DMSO control and AhR antagonist/agonist treated cells was analysed by one-way ANOVA. ***, p
    Figure Legend Snippet: The effect of AhR modulation on Th17 and Tc17 cell frequency. Naïve CD4 + cells from AhR +/− (A and E) or AhR −/− mice (B and F) and naïve CD8 + cells from AhR +/− (C and G) or AhR −/− mice (D and H) were polarised under Th17/Tc17 conditions for 5 days. Cells were then stimulated with PdBU and ionomycin in the presence of brefeldin A. The polarised cells were then permeabilised and stained using fluorescent anti-IL-17A (PE [Y-axis]) and -IFN-γ (APC [X-axis]) labelled antibodies. Cells (25000) were analysed by flow cytometry. The cells were cultured in the presence of AhR antagonist (CH-223191) (white bar) or AhR agonist (FICZ) (grey bar) both formulated in DMSO or with an equivalent amount of DMSO alone (black bar). Representative quadrant analyses are illustrated (A–D). The percentage of cells positive for IL-17, IL-17 and IFN-γ or IFN-γ alone was calculated by subtracting the isotype controls from the positive cells in each quadrant and are illustrated as % positive cells (E-H; mean ± SE; n = 3 independent experiments). Statistical significance of differences between DMSO control and AhR antagonist/agonist treated cells was analysed by one-way ANOVA. ***, p

    Techniques Used: Mouse Assay, Staining, Flow Cytometry, Cytometry, Cell Culture

    7) Product Images from "Differential expression of IL-17A and IL-17F is coupled to TCR signaling via Itk-mediated regulation of NFATc1"

    Article Title: Differential expression of IL-17A and IL-17F is coupled to TCR signaling via Itk-mediated regulation of NFATc1

    Journal: Immunity

    doi: 10.1016/j.immuni.2009.07.009

    IL-17A production is affected by TCR and NFAT activation
    Figure Legend Snippet: IL-17A production is affected by TCR and NFAT activation

    Techniques Used: Activation Assay

    Reduced IL-17A production from Itk −/− and Itk −/− Rlk −/− CD4 + T cells
    Figure Legend Snippet: Reduced IL-17A production from Itk −/− and Itk −/− Rlk −/− CD4 + T cells

    Techniques Used:

    Itk is required for efficient transcription of IL-17A , but not Il-17F
    Figure Legend Snippet: Itk is required for efficient transcription of IL-17A , but not Il-17F

    Techniques Used:

    Itk −/− mice show impaired production of IL-17A in vivo
    Figure Legend Snippet: Itk −/− mice show impaired production of IL-17A in vivo

    Techniques Used: Mouse Assay, In Vivo

    IL-17A production in Itk −/− CD4 + T cells is reduced in response to multiple cytokines, yet normal expression of RORγT and RORα
    Figure Legend Snippet: IL-17A production in Itk −/− CD4 + T cells is reduced in response to multiple cytokines, yet normal expression of RORγT and RORα

    Techniques Used: Expressing

    IL-17A expression is linked to NFAT activation
    Figure Legend Snippet: IL-17A expression is linked to NFAT activation

    Techniques Used: Expressing, Activation Assay

    The IL-17 locus has an open chromatin conformation: caNFATc1 rescues IL-17A defect in Itk −/− cells
    Figure Legend Snippet: The IL-17 locus has an open chromatin conformation: caNFATc1 rescues IL-17A defect in Itk −/− cells

    Techniques Used:

    8) Product Images from "Differential expression of IL-17A and IL-17F is coupled to TCR signaling via Itk-mediated regulation of NFATc1"

    Article Title: Differential expression of IL-17A and IL-17F is coupled to TCR signaling via Itk-mediated regulation of NFATc1

    Journal: Immunity

    doi: 10.1016/j.immuni.2009.07.009

    IL-17A production is affected by TCR and NFAT activation
    Figure Legend Snippet: IL-17A production is affected by TCR and NFAT activation

    Techniques Used: Activation Assay

    Reduced IL-17A production from Itk −/− and Itk −/− Rlk −/− CD4 + T cells
    Figure Legend Snippet: Reduced IL-17A production from Itk −/− and Itk −/− Rlk −/− CD4 + T cells

    Techniques Used:

    Itk is required for efficient transcription of IL-17A , but not Il-17F
    Figure Legend Snippet: Itk is required for efficient transcription of IL-17A , but not Il-17F

    Techniques Used:

    Itk −/− mice show impaired production of IL-17A in vivo
    Figure Legend Snippet: Itk −/− mice show impaired production of IL-17A in vivo

    Techniques Used: Mouse Assay, In Vivo

    IL-17A production in Itk −/− CD4 + T cells is reduced in response to multiple cytokines, yet normal expression of RORγT and RORα
    Figure Legend Snippet: IL-17A production in Itk −/− CD4 + T cells is reduced in response to multiple cytokines, yet normal expression of RORγT and RORα

    Techniques Used: Expressing

    IL-17A expression is linked to NFAT activation
    Figure Legend Snippet: IL-17A expression is linked to NFAT activation

    Techniques Used: Expressing, Activation Assay

    The IL-17 locus has an open chromatin conformation: caNFATc1 rescues IL-17A defect in Itk −/− cells
    Figure Legend Snippet: The IL-17 locus has an open chromatin conformation: caNFATc1 rescues IL-17A defect in Itk −/− cells

    Techniques Used:

    9) Product Images from "Complement dependency of cardiomyocyte release of mediators during sepsis"

    Article Title: Complement dependency of cardiomyocyte release of mediators during sepsis

    Journal: The FASEB Journal

    doi: 10.1096/fj.11-183236

    Cytokines (TNFα, IL-6) and chemokines (MIP-1α, MIP-2) released from sham-treated mouse CMs and from 24 h CLP CMs obtained from WT mice administered control IgG, anti-C5a (40 μg), or anti-IL-17A IgG (50 μg), all administered
    Figure Legend Snippet: Cytokines (TNFα, IL-6) and chemokines (MIP-1α, MIP-2) released from sham-treated mouse CMs and from 24 h CLP CMs obtained from WT mice administered control IgG, anti-C5a (40 μg), or anti-IL-17A IgG (50 μg), all administered

    Techniques Used: Mouse Assay

    10) Product Images from "TGF-β inhibitor Smad7 regulates dendritic cell-induced autoimmunity"

    Article Title: TGF-β inhibitor Smad7 regulates dendritic cell-induced autoimmunity

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

    doi: 10.1073/pnas.1615065114

    Inhibition of IDO by 1-MT restores susceptibility of S7 ΔDC mice to EAE. ( A ) Relative expression of IDO1 and IDO2 in purified splenic CD11c + DCs isolated from S7 ΔDC ( n = 2) and control mice ( n = 2) left untreated or stimulated for 12 h or 24 h with 10 ng/mL IFN-γ. IDO1 and IDO2 expression levels were normalized to the respective controls. ( B ) IDO1 (MFI) of iLN-derived CD11c + MHC-II + , CD11c + MHCII + CD8 + , CD11c + MHC-II + CD11b + , and CD11c + MHC-II + CD8 + CD103 + DCs pregated on viable CD90.2 − B220 − cells of control ( n = 4) and S7 ΔDC ( n = 4) mice on day 5 after EAE induction. ( C ) EAE disease progression in vehicle-treated control ( n = 3) and S7 ΔDC ( n = 4) mice and 1-MT–treated control ( n = 5) and S7 ΔDC ( n = 3) mice. Vehicle or 1-MT treatment was performed once on the day of MOG 35–55 /CFA immunization. One representative of two independent experiments is shown. ( D ) Analysis of CNS infiltrates on day 20 after EAE induction in mice treated with vehicle or 1-MT from B . FACS blots illustrating CNS-infiltrating CD45.2 + CD11b − lymphocytes pregated on viable cells ( Upper ), CD90.2 + CD4 + cells pregated on viable cells ( Upper Middle ), MOG-specific CD40L + CD44 + effector T cells pregated on viable CD90.2 + CD4 + cells ( Lower Middle ), and MOG-specific Th1, Th17, and IL-17A + IFNγ + double-producing cells as gated on viable CD90.2 + CD4 + CD40L + CD44 + cells ( Lower ). ( E ) Analysis of CD4 + FoxP3 + Treg numbers in LNs from naïve control mice ( n = 3) as well as EAE-immunized mice 10 d after immunization treated with vehicle [control ( n = 8); S7 ΔDC ( n = 8)] or 1-MT [control ( n = 5); S7 ΔDC ( n = 6)] on the day of EAE immunization. Cells were gated on viable CD90.2 + CD4 + cells. ( A , B , D and E ) One experiment is depicted. Bar graphs represent mean value ± SEM. Statistical significance was assessed by Student’s t test ( A , B , and E ), EAE AUC followed by two-way ANOVA and Bonferroni posttests ( C ), or two-way ANOVA and Bonferroni posttests ( D ) (* P ≤ 0.05, ** P ≤ 0.005, and *** P ≤ 0.0005).
    Figure Legend Snippet: Inhibition of IDO by 1-MT restores susceptibility of S7 ΔDC mice to EAE. ( A ) Relative expression of IDO1 and IDO2 in purified splenic CD11c + DCs isolated from S7 ΔDC ( n = 2) and control mice ( n = 2) left untreated or stimulated for 12 h or 24 h with 10 ng/mL IFN-γ. IDO1 and IDO2 expression levels were normalized to the respective controls. ( B ) IDO1 (MFI) of iLN-derived CD11c + MHC-II + , CD11c + MHCII + CD8 + , CD11c + MHC-II + CD11b + , and CD11c + MHC-II + CD8 + CD103 + DCs pregated on viable CD90.2 − B220 − cells of control ( n = 4) and S7 ΔDC ( n = 4) mice on day 5 after EAE induction. ( C ) EAE disease progression in vehicle-treated control ( n = 3) and S7 ΔDC ( n = 4) mice and 1-MT–treated control ( n = 5) and S7 ΔDC ( n = 3) mice. Vehicle or 1-MT treatment was performed once on the day of MOG 35–55 /CFA immunization. One representative of two independent experiments is shown. ( D ) Analysis of CNS infiltrates on day 20 after EAE induction in mice treated with vehicle or 1-MT from B . FACS blots illustrating CNS-infiltrating CD45.2 + CD11b − lymphocytes pregated on viable cells ( Upper ), CD90.2 + CD4 + cells pregated on viable cells ( Upper Middle ), MOG-specific CD40L + CD44 + effector T cells pregated on viable CD90.2 + CD4 + cells ( Lower Middle ), and MOG-specific Th1, Th17, and IL-17A + IFNγ + double-producing cells as gated on viable CD90.2 + CD4 + CD40L + CD44 + cells ( Lower ). ( E ) Analysis of CD4 + FoxP3 + Treg numbers in LNs from naïve control mice ( n = 3) as well as EAE-immunized mice 10 d after immunization treated with vehicle [control ( n = 8); S7 ΔDC ( n = 8)] or 1-MT [control ( n = 5); S7 ΔDC ( n = 6)] on the day of EAE immunization. Cells were gated on viable CD90.2 + CD4 + cells. ( A , B , D and E ) One experiment is depicted. Bar graphs represent mean value ± SEM. Statistical significance was assessed by Student’s t test ( A , B , and E ), EAE AUC followed by two-way ANOVA and Bonferroni posttests ( C ), or two-way ANOVA and Bonferroni posttests ( D ) (* P ≤ 0.05, ** P ≤ 0.005, and *** P ≤ 0.0005).

    Techniques Used: Inhibition, Mouse Assay, Expressing, Purification, Isolation, Derivative Assay, FACS

    DC-specific Smad7 deletion renders mice resistant to EAE. ( A ) EAE disease course of S7 ΔDC ( n = 10) and control animals ( n = 8) after MOG 35–55 /CFA and PTX immunization. One representative of five independent experiments is shown. ( B ) Flow cytometric analysis of CNS-infiltrating CD90.2 + T cells from S7 ΔDC ( n = 8) and control mice ( n = 7) at the peak of disease (day 15). Cells were gated on live cells. One representative of four independent experiments is depicted. ( C ) FACS blots of CNS-infiltrating CD4 + T cells from S7 ΔDC ( n = 8) and control mice ( n = 7) at the peak of disease (day 15; Upper ). MOG 35–55 –specific CNS-infiltrating effector T cells (CD40L high CD44 + ) pregated on CD90.2 + CD4 + cells ( Middle ). MOG 35–55 –specific CNS-infiltrating Th1 (IFN-γ + ) and Th17 (IL-17A + ) effector cells were pregated on CD90.2 + CD4 + CD40L high CD44 + cells ( Lower ). ( D ) Percentage and total cell counts of CNS-infiltrating FoxP3 + Tregs ( Upper ) and LN and splenic Foxp3 + Tregs of S7 ΔDC ( n = 8) and control mice ( n = 7) at the peak of disease (day 15; Middle and Lower , respectively). One representative of four independent experiments is depicted. Bar graphs depict mean value ± SEM. Statistical significance was assessed by using ( A ) EAE AUC followed by Student’s t test and ( B – D ) Student’s t test (* P ≤ 0.05, ** P ≤ 0.005, and *** P ≤ 0.0005).
    Figure Legend Snippet: DC-specific Smad7 deletion renders mice resistant to EAE. ( A ) EAE disease course of S7 ΔDC ( n = 10) and control animals ( n = 8) after MOG 35–55 /CFA and PTX immunization. One representative of five independent experiments is shown. ( B ) Flow cytometric analysis of CNS-infiltrating CD90.2 + T cells from S7 ΔDC ( n = 8) and control mice ( n = 7) at the peak of disease (day 15). Cells were gated on live cells. One representative of four independent experiments is depicted. ( C ) FACS blots of CNS-infiltrating CD4 + T cells from S7 ΔDC ( n = 8) and control mice ( n = 7) at the peak of disease (day 15; Upper ). MOG 35–55 –specific CNS-infiltrating effector T cells (CD40L high CD44 + ) pregated on CD90.2 + CD4 + cells ( Middle ). MOG 35–55 –specific CNS-infiltrating Th1 (IFN-γ + ) and Th17 (IL-17A + ) effector cells were pregated on CD90.2 + CD4 + CD40L high CD44 + cells ( Lower ). ( D ) Percentage and total cell counts of CNS-infiltrating FoxP3 + Tregs ( Upper ) and LN and splenic Foxp3 + Tregs of S7 ΔDC ( n = 8) and control mice ( n = 7) at the peak of disease (day 15; Middle and Lower , respectively). One representative of four independent experiments is depicted. Bar graphs depict mean value ± SEM. Statistical significance was assessed by using ( A ) EAE AUC followed by Student’s t test and ( B – D ) Student’s t test (* P ≤ 0.05, ** P ≤ 0.005, and *** P ≤ 0.0005).

    Techniques Used: Mouse Assay, Flow Cytometry, FACS

    11) Product Images from "Lymphoid tissue inducer-like cells are an innate source of IL-17 and IL-22"

    Article Title: Lymphoid tissue inducer-like cells are an innate source of IL-17 and IL-22

    Journal: The Journal of Experimental Medicine

    doi: 10.1084/jem.20072713

    Zymosan induces IL-17 production in splenic LTi-like cells in vivo. (left) Intracellular staining of IL-17A was performed with in vitro conventional staining (top) or in vivo staining (bottom). For conventional staining, Rag2 −/− mice were challenged with PBS (Control) or 12.5 mg zymosan i.p. Splenocytes were isolated 2 h later and stimulated with PMA/Iono and BFA for 2 h in vitro. The proportion of IL-17A–producing LTi-like cells was evaluated by intracellular staining. For the in vivo staining, Rag2 −/− mice were injected with PBS (Control) or 12.5 mg zymosan i.p. together with 0.25 mg BFA i.v. (reference 22 ). The proportion of IL-17A–producing LTi-like cells in spleens was directly evaluated by intracellular staining. (right) The mean values (horizontal bars) for IL-17A–producing LTi-like cells were calculated for in vitro staining (top, n = 6) and in vivo staining (bottom, n = 6). Data are representative of three (top) or two (bottom) independent experiments. ***, P
    Figure Legend Snippet: Zymosan induces IL-17 production in splenic LTi-like cells in vivo. (left) Intracellular staining of IL-17A was performed with in vitro conventional staining (top) or in vivo staining (bottom). For conventional staining, Rag2 −/− mice were challenged with PBS (Control) or 12.5 mg zymosan i.p. Splenocytes were isolated 2 h later and stimulated with PMA/Iono and BFA for 2 h in vitro. The proportion of IL-17A–producing LTi-like cells was evaluated by intracellular staining. For the in vivo staining, Rag2 −/− mice were injected with PBS (Control) or 12.5 mg zymosan i.p. together with 0.25 mg BFA i.v. (reference 22 ). The proportion of IL-17A–producing LTi-like cells in spleens was directly evaluated by intracellular staining. (right) The mean values (horizontal bars) for IL-17A–producing LTi-like cells were calculated for in vitro staining (top, n = 6) and in vivo staining (bottom, n = 6). Data are representative of three (top) or two (bottom) independent experiments. ***, P

    Techniques Used: In Vivo, Staining, In Vitro, Mouse Assay, Isolation, Injection

    Isolated CD4 + CD3 − CD11c − B220 − LTi-like cells produce IL-17 and constitutively express IL-23R, RORγt, AHR, and CCR6. (A) Isolated CD4 + CD3 − CD11c − B220 − LTi-like subsets from Rag2 −/− splenocytes (top) were cultured in the absence (Control) or presence of IL-23 (or with PMA/Iono) for 24 h, and IL-17A in culture supernatants was measured by ELISA (bottom). Data are means ± SD from duplicate cultures and are representative of two independent experiments. (B) Stat3 fl/fl or Stat3 fl/fl ; MMTV-Cre splenocytes were cultured in the absence (Control) or presence of IL-23 for 24 h. The proportion of IL-17A–producing LTi-like cells was evaluated by intracellular staining. Data are means ± SD from duplicate cultures and are representative of four independent experiments ( n = 8). *, P
    Figure Legend Snippet: Isolated CD4 + CD3 − CD11c − B220 − LTi-like cells produce IL-17 and constitutively express IL-23R, RORγt, AHR, and CCR6. (A) Isolated CD4 + CD3 − CD11c − B220 − LTi-like subsets from Rag2 −/− splenocytes (top) were cultured in the absence (Control) or presence of IL-23 (or with PMA/Iono) for 24 h, and IL-17A in culture supernatants was measured by ELISA (bottom). Data are means ± SD from duplicate cultures and are representative of two independent experiments. (B) Stat3 fl/fl or Stat3 fl/fl ; MMTV-Cre splenocytes were cultured in the absence (Control) or presence of IL-23 for 24 h. The proportion of IL-17A–producing LTi-like cells was evaluated by intracellular staining. Data are means ± SD from duplicate cultures and are representative of four independent experiments ( n = 8). *, P

    Techniques Used: Isolation, Cell Culture, Enzyme-linked Immunosorbent Assay, Staining

    IL-23 and zymosan induce IL-17 production in a population of non–B, non–T cells. (A) WT or Rag2 −/− splenocytes were cultured in the presence of the indicated cytokines for 48 h, and IL-17A in culture supernatants was measured by ELISA. The data are means ± SD from duplicate cultures and are representative of four independent experiments ( n = 8). **, P
    Figure Legend Snippet: IL-23 and zymosan induce IL-17 production in a population of non–B, non–T cells. (A) WT or Rag2 −/− splenocytes were cultured in the presence of the indicated cytokines for 48 h, and IL-17A in culture supernatants was measured by ELISA. The data are means ± SD from duplicate cultures and are representative of four independent experiments ( n = 8). **, P

    Techniques Used: Cell Culture, Enzyme-linked Immunosorbent Assay

    CD4 + CD3 − lineage − cells produce IL-17. Rag2 −/− splenocytes were cultured in the absence (Control) or presence of IL-23 for 24 h. The proportion of IL-17A–producing CD3 − cells was evaluated by intracellular staining. (A) NK1.1 + versus IL-17A + cells gated on CD3 − cells are shown. (B) IL-17A + versus CD3 + cells (nongated; left) and IL-17A + versus CD4 + cells gated on CD3 − cells (right) are shown. Data are representative of three independent experiments.
    Figure Legend Snippet: CD4 + CD3 − lineage − cells produce IL-17. Rag2 −/− splenocytes were cultured in the absence (Control) or presence of IL-23 for 24 h. The proportion of IL-17A–producing CD3 − cells was evaluated by intracellular staining. (A) NK1.1 + versus IL-17A + cells gated on CD3 − cells are shown. (B) IL-17A + versus CD3 + cells (nongated; left) and IL-17A + versus CD4 + cells gated on CD3 − cells (right) are shown. Data are representative of three independent experiments.

    Techniques Used: Cell Culture, Staining

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    Article Snippet: Total protein level was determined by using BCA Protein Assay Kit (Thermo Fisher Scientific, Rockford, IL, USA) according to the manufacturers' instructions. .. 2.6 Enzyme-linked immunosorbent assay (ELISA) IL-1β, IL-10, IL-17A and IFN-γ in lung tissues and BAL fluid were measured using ELISA kits for mouse IL-1β and IL-10 (R & D Systems, Minneapolis, USA) and ELISA Ready-Set-Go kit for mouse IL-17A and IFN-γ (eBioscience, San Diego, CA, USA), respectively, following the manufacturers' instructions. .. 2.7 Histology and immunohistochemistry Paraformaldehyde-fixed, paraffin-embedded lung tissues were sectioned for hematoxylin and eosin staining and immunohistochemical staining of F4/80 (Abcam, Cambridge, UK) and IL-1β (Santa Cruz Biotechnology, Dallas, Texas, USA).

    Article Title: Soluble IL-2R? (sCD25) Exacerbates Autoimmunity and Enhances the Development of Th17 Responses in Mice
    Article Snippet: .. Materials ELISA kits for mouse IL-17A, IFNγ, IL-2 and IL-22 were purchased from ebioscience (Hatfield UK). .. ELISA kit for sCD25 was purchased from R & D systems (Abingdon, UK) Recombinant murine sCD25His was purchased from R & D systems.

    Article Title: Intrinsically altered lung‐resident γδT cells control lung melanoma by producing interleukin‐17A in the elderly, et al. Intrinsically altered lung‐resident γδT cells control lung melanoma by producing interleukin‐17A in the elderly
    Article Snippet: 4.7 In vitro cytotoxicity assay The cytotoxicity of γδT cells against B16/F10 cells was measured using the CellTrace™ Far Red Kit (Invitrogen) according to the instructions provided by the manufacturer. .. 4.8 Detection of IL‐17A protein The expression levels of IL‐17A protein in the serum and lung homogenate were detected using a mouse IL‐17A enzyme‐linked immunosorbent assay (ELISA) kit (eBioscience). .. Lung samples were homogenized in buffer containing Triton X‐100 and a protease inhibitor cocktail (Complete Mini; Roche).

    Article Title: Effects of Bu Shen Yi Sui Capsule on Th17/Treg cytokines in C57BL/6 mice with experimental autoimmune encephalomyelitis
    Article Snippet: Complete Freund’ adjuvant (CFA) and pertussis toxin (PTX) were purchased by Sigma-Aldrich (St. Louis, MO, USA). .. Enzyme-linked immunosorbent assay (ELISA) kits for mouse IL-17A was purchased from eBioScience (San Diego, CA, USA), mouse IL-23 was from Beijing 4A Biotech Co., Ltd. (Beijing, China), mouse IL-6 and mouse TGF-β1 were provided by NeoBioscience Technology Co. (Beijing, China). .. Mouse anti-IL-17A PERCP-CY5.5, mouse anti-CD4 APC, mouse anti-CD25 FITC, anti-mouse/rat FoxP3 PE, rat IgG isotypecontrol PE, FoxP3 staining buffer set, phorbol 12-myristate 13-acetate (PMA), ionomycin, and brefeldin A solution were purchased from BD PharMingen (San Diego, CA, USA).

    Article Title: Expression of Interleukin-17A in Lung Tissues of Irradiated Mice and the Influence of Dexamethasone
    Article Snippet: Animals and Reagents Inbred male C57BL/6J mice (21 ± 2 g, 6–8 weeks) were obtained from Vital River Laboratory Animal Technology. .. The ELISA assay kits for mouse IL-17A, TGF-β 1, TNF-α , and IL-6 were purchased from eBioscience (San Diego, CA, USA). .. The mouse IL-17A polyclonal Ab for immunohistochemical analysis was obtained from Abcam (Abcam Inc., Cambridge, MA, USA).

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    Expressing:

    Article Title: Intrinsically altered lung‐resident γδT cells control lung melanoma by producing interleukin‐17A in the elderly, et al. Intrinsically altered lung‐resident γδT cells control lung melanoma by producing interleukin‐17A in the elderly
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    Thermo Fisher anti il 17a
    EC sensitization elicits a systemic IL-22 response and an antigen-specific IL-22 response in the lungs A-B. IL-22 secretion by OVA stimulated splenocytes (A) and IL-22 serum levels (B). C,D . Il22 mRNA expression in the lungs (C), and IL-22 secretion by OVA stimulated lung cells (D). E. Representative FACS analysis and quantitation of intracelluar expression of IL-22 + cells among CD3 + CD4 + T cells and of <t>IL-17A</t> + and TNFα + cells among CD3 + CD4 + IL-22 + cells in the lung. Mice were EC sensitized with OVA or saline in A and B, followed by i.n. challenged with OVA in C-F. Bars represent mean±SEM (n=5–10 per group). *p
    Anti Il 17a, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Thermo Fisher gene exp il17a mm00439618 m1
    Cytokine gene expression in the tissues of Normal diet (ND)-, High fat diet (HD)-, and Paigen diet (PD)-fed mice. Single cell suspensions were prepared from solid tissues (aorta, heart, and abdominal fat), and used for total RNA extraction and for qPCR. Relative quantification of <t>IL-17A,</t> IFN-γ, IL-4, TGF-β, IL-1α, IL-12, and IL-6 mRNA levels were performed using the comparative CT method with normalization to GAPDH; results were expressed as fold difference relative to a relevant control sample. (A) <t>IL-17</t> mRNA levels in the aorta, heart and adipose tissue. (B) IFN-γ and IL-4 mRNA levels in the aorta. (C) IL-1α, IFN-γ, and IL-4 mRNA levels in the heart. (D) IL-6 and IL-12 mRNA levels in the adipose tissue. N = 3–4. * p
    Gene Exp Il17a Mm00439618 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Thermo Fisher gene exp il17a mm00439619 m1
    IL-20R signaling suppresses <t>IL-17A</t> response to S. aureus infection ( a-b ) mRNA expression in infected skin compared to uninfected control at indicated time points after MRSA infection. ( c ) IL-17A mRNA expression compared to uninfected control two hours and six days after infection in wild type (WT), Il20rb −/− , or recombinant cytokine-treated wild type mice. ( d-g ) IL-17A and CD45 staining of live cells from ear skin of wild type mice two hours after injection ( d-e ) or flank skin of wild type mice four days after injection ( f-g ) with PBS (uninfected, UI), MRSA, or MRSA + rmIL-19. Representative plots ( d, f ) and absolute cell numbers from replicate mice ( e, g ) are shown. ( h-i ) Lesion size and bacterial CFU (six days after infection) in wild type (WT) or Il20rb −/− mice injected with control or IL-17A-neutralizing antibody (α-IL-17A) at the time of MRSA inoculation. Data shown are representative of 2-4 independent experiments, each using 3-5 mice per group, and displayed as mean + s.e.m. or representative flow cytometry plots.
    Gene Exp Il17a Mm00439619 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/gene exp il17a mm00439619 m1/product/Thermo Fisher
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    Image Search Results


    EC sensitization elicits a systemic IL-22 response and an antigen-specific IL-22 response in the lungs A-B. IL-22 secretion by OVA stimulated splenocytes (A) and IL-22 serum levels (B). C,D . Il22 mRNA expression in the lungs (C), and IL-22 secretion by OVA stimulated lung cells (D). E. Representative FACS analysis and quantitation of intracelluar expression of IL-22 + cells among CD3 + CD4 + T cells and of IL-17A + and TNFα + cells among CD3 + CD4 + IL-22 + cells in the lung. Mice were EC sensitized with OVA or saline in A and B, followed by i.n. challenged with OVA in C-F. Bars represent mean±SEM (n=5–10 per group). *p

    Journal: The Journal of allergy and clinical immunology

    Article Title: IL-22 promotes allergic airway inflammation in epicutaneously sensitized mice

    doi: 10.1016/j.jaci.2018.05.032

    Figure Lengend Snippet: EC sensitization elicits a systemic IL-22 response and an antigen-specific IL-22 response in the lungs A-B. IL-22 secretion by OVA stimulated splenocytes (A) and IL-22 serum levels (B). C,D . Il22 mRNA expression in the lungs (C), and IL-22 secretion by OVA stimulated lung cells (D). E. Representative FACS analysis and quantitation of intracelluar expression of IL-22 + cells among CD3 + CD4 + T cells and of IL-17A + and TNFα + cells among CD3 + CD4 + IL-22 + cells in the lung. Mice were EC sensitized with OVA or saline in A and B, followed by i.n. challenged with OVA in C-F. Bars represent mean±SEM (n=5–10 per group). *p

    Article Snippet: Cells were then fixed and permeabilized using BD Cytofix/Cytoperm Kit (BD Biosciences) and stained with anti-IL-22 (Biolegend), anti-TNFα (Biolegend), anti-IL-17A (eBioscience) or anti-IFNγ (eBioscience) antibodies..

    Techniques: Expressing, FACS, Quantitation Assay, Mouse Assay

    Cytokine gene expression in the tissues of Normal diet (ND)-, High fat diet (HD)-, and Paigen diet (PD)-fed mice. Single cell suspensions were prepared from solid tissues (aorta, heart, and abdominal fat), and used for total RNA extraction and for qPCR. Relative quantification of IL-17A, IFN-γ, IL-4, TGF-β, IL-1α, IL-12, and IL-6 mRNA levels were performed using the comparative CT method with normalization to GAPDH; results were expressed as fold difference relative to a relevant control sample. (A) IL-17 mRNA levels in the aorta, heart and adipose tissue. (B) IFN-γ and IL-4 mRNA levels in the aorta. (C) IL-1α, IFN-γ, and IL-4 mRNA levels in the heart. (D) IL-6 and IL-12 mRNA levels in the adipose tissue. N = 3–4. * p

    Journal: Frontiers in Microbiology

    Article Title: Gut Dysbiosis and Adaptive Immune Response in Diet-induced Obesity vs. Systemic Inflammation

    doi: 10.3389/fmicb.2017.01157

    Figure Lengend Snippet: Cytokine gene expression in the tissues of Normal diet (ND)-, High fat diet (HD)-, and Paigen diet (PD)-fed mice. Single cell suspensions were prepared from solid tissues (aorta, heart, and abdominal fat), and used for total RNA extraction and for qPCR. Relative quantification of IL-17A, IFN-γ, IL-4, TGF-β, IL-1α, IL-12, and IL-6 mRNA levels were performed using the comparative CT method with normalization to GAPDH; results were expressed as fold difference relative to a relevant control sample. (A) IL-17 mRNA levels in the aorta, heart and adipose tissue. (B) IFN-γ and IL-4 mRNA levels in the aorta. (C) IL-1α, IFN-γ, and IL-4 mRNA levels in the heart. (D) IL-6 and IL-12 mRNA levels in the adipose tissue. N = 3–4. * p

    Article Snippet: Primers and probes were from Qiagen: GAPDH (Mm99999915_g1), IL-17A (Mm00439618_m1), IFN-γ (Mm01168134_m1), IL-4 (Mm00445259_m1), TGF-β (Mm01178820_m1), IL-6 (Mm00446190_m1), IL-12 p35 (Mm00434165_m1).

    Techniques: Expressing, Mouse Assay, RNA Extraction, Real-time Polymerase Chain Reaction

    IL-20R signaling suppresses IL-17A response to S. aureus infection ( a-b ) mRNA expression in infected skin compared to uninfected control at indicated time points after MRSA infection. ( c ) IL-17A mRNA expression compared to uninfected control two hours and six days after infection in wild type (WT), Il20rb −/− , or recombinant cytokine-treated wild type mice. ( d-g ) IL-17A and CD45 staining of live cells from ear skin of wild type mice two hours after injection ( d-e ) or flank skin of wild type mice four days after injection ( f-g ) with PBS (uninfected, UI), MRSA, or MRSA + rmIL-19. Representative plots ( d, f ) and absolute cell numbers from replicate mice ( e, g ) are shown. ( h-i ) Lesion size and bacterial CFU (six days after infection) in wild type (WT) or Il20rb −/− mice injected with control or IL-17A-neutralizing antibody (α-IL-17A) at the time of MRSA inoculation. Data shown are representative of 2-4 independent experiments, each using 3-5 mice per group, and displayed as mean + s.e.m. or representative flow cytometry plots.

    Journal: Nature immunology

    Article Title: IL-20 receptor signaling inhibits cutaneous IL-1? and IL-17A production to promote methicillin-resistant Staphylococcus aureus infection

    doi: 10.1038/ni.2637

    Figure Lengend Snippet: IL-20R signaling suppresses IL-17A response to S. aureus infection ( a-b ) mRNA expression in infected skin compared to uninfected control at indicated time points after MRSA infection. ( c ) IL-17A mRNA expression compared to uninfected control two hours and six days after infection in wild type (WT), Il20rb −/− , or recombinant cytokine-treated wild type mice. ( d-g ) IL-17A and CD45 staining of live cells from ear skin of wild type mice two hours after injection ( d-e ) or flank skin of wild type mice four days after injection ( f-g ) with PBS (uninfected, UI), MRSA, or MRSA + rmIL-19. Representative plots ( d, f ) and absolute cell numbers from replicate mice ( e, g ) are shown. ( h-i ) Lesion size and bacterial CFU (six days after infection) in wild type (WT) or Il20rb −/− mice injected with control or IL-17A-neutralizing antibody (α-IL-17A) at the time of MRSA inoculation. Data shown are representative of 2-4 independent experiments, each using 3-5 mice per group, and displayed as mean + s.e.m. or representative flow cytometry plots.

    Article Snippet: Mouse primers were all purchased from Applied Biosystems, Life Technologies: IL-17A (Mm00439619_m1*), IL-17F (Mm00521423_m1*), IL-22 (Mm00444241_m1), DefB4 (Mm00731768_m1*), IL-19 (Mm01288324_m1*), IL-20 (Mm00445341_m1*), IL-24 (Mm00474102_m1*), IL-20RA (Mm00555504_m1*), IL-20RB (Mm01232398_m1*), IL-22Ra1 (Mm01192943_m1*), IL-12(p40) (Mm99999067_m1), interferon gamma (Mm01168134_m1*), IL-1β (Mm01336189_m1*), IL-6 (Mm00446190_m1*), IL-23(p19) (Mm00518984_m1*), TLR2 (Mm00445212_m1*), IL-1Ra (Mm00446186_m1*), IL-1R1(Mm00434237_m1*), IL-1R2 (Mm00439629_m1*), Beta-defens in 4 (Mm01184338_m1*), S100a8 (Mm00496696_g1*), and S100a9 (Mm00656925_m1*).

    Techniques: Infection, Expressing, Recombinant, Mouse Assay, Staining, Injection, Flow Cytometry, Cytometry

    Recombinant IL-1β rescues IL-20R cytokine-induced susceptibility to S. aureus ( a ) IL-1β expression in live CD104 + keratinocytes detected by flow cytometry of single cell suspensions from infected skin tissue three days after MRSA infection with or without (PBS) recombinant murine cytokine (rmIL-19, rmIL-20) treatment. Staining of uninfected skin (UI) and staining with isotype control antibody also shown. ( b-d ) Wild type mice were inoculated with MRSA in PBS, rmIL-19, or rmIL-19 + rmIL-1β and assessed for lesion size ( b ), bacterial burden ( c ), and IL-17A mRNA ( d ). ( e ) IL-19 and IL-24 mRNA expression in Il17a −/− and Il1r1 −/− mice, normalized to wild type (WT) mice, six days after infection with MRSA. Data shown are representative of 2-3 independent experiments, using at least 3-5 mice per group each time, and displayed as mean + s.e.m.

    Journal: Nature immunology

    Article Title: IL-20 receptor signaling inhibits cutaneous IL-1? and IL-17A production to promote methicillin-resistant Staphylococcus aureus infection

    doi: 10.1038/ni.2637

    Figure Lengend Snippet: Recombinant IL-1β rescues IL-20R cytokine-induced susceptibility to S. aureus ( a ) IL-1β expression in live CD104 + keratinocytes detected by flow cytometry of single cell suspensions from infected skin tissue three days after MRSA infection with or without (PBS) recombinant murine cytokine (rmIL-19, rmIL-20) treatment. Staining of uninfected skin (UI) and staining with isotype control antibody also shown. ( b-d ) Wild type mice were inoculated with MRSA in PBS, rmIL-19, or rmIL-19 + rmIL-1β and assessed for lesion size ( b ), bacterial burden ( c ), and IL-17A mRNA ( d ). ( e ) IL-19 and IL-24 mRNA expression in Il17a −/− and Il1r1 −/− mice, normalized to wild type (WT) mice, six days after infection with MRSA. Data shown are representative of 2-3 independent experiments, using at least 3-5 mice per group each time, and displayed as mean + s.e.m.

    Article Snippet: Mouse primers were all purchased from Applied Biosystems, Life Technologies: IL-17A (Mm00439619_m1*), IL-17F (Mm00521423_m1*), IL-22 (Mm00444241_m1), DefB4 (Mm00731768_m1*), IL-19 (Mm01288324_m1*), IL-20 (Mm00445341_m1*), IL-24 (Mm00474102_m1*), IL-20RA (Mm00555504_m1*), IL-20RB (Mm01232398_m1*), IL-22Ra1 (Mm01192943_m1*), IL-12(p40) (Mm99999067_m1), interferon gamma (Mm01168134_m1*), IL-1β (Mm01336189_m1*), IL-6 (Mm00446190_m1*), IL-23(p19) (Mm00518984_m1*), TLR2 (Mm00445212_m1*), IL-1Ra (Mm00446186_m1*), IL-1R1(Mm00434237_m1*), IL-1R2 (Mm00439629_m1*), Beta-defens in 4 (Mm01184338_m1*), S100a8 (Mm00496696_g1*), and S100a9 (Mm00656925_m1*).

    Techniques: Recombinant, Expressing, Flow Cytometry, Cytometry, Infection, Staining, Mouse Assay

    Linking gut and spleen IL-17 cells (A) SI-LP lymphocytes were isolated from SPF or GF K/BxN mice. Cells were stained, analyzed by flow cytometry and gated as indicated. Expression of IL-17 versus CCR6 is plotted. The values indicate percentages of IL-17 + CCR6 + cells in CD3 + CD4 + B220 − cells. Data are representative of three independent experiments. (B) SI-LP lymphocytes (i) and splenocytes (ii) were isolated from SPF mice of the indicated ages, stained and analyzed by flow cytometry, gated as indicated. Plots displayed IL-17 versus CCR6 expression. Values indicate % of IL-17 + CCR6 + cells in total CD4 + T cells (CD3 + CD4 + B220 − ). Data are representative of two independent experiments. (iii) Measurement of ankle thickening for the same mice. Each circle represents one animal from two independent experiments. (C) Splenocytes from SPF BxN or K/BxN mice were stained and analyzed by flow cytometry, gated as indicated. Plots depict IL-17 versus α4β7 staining. Values indicate % of IL-17 + α4β7 + or IL-17 + α4β7 − cells in total CD4 + T cells (CD3 + CD4 + B220 − ). Data are representative of two independent experiments.

    Journal: Immunity

    Article Title: Gut-residing segmented filamentous bacteria drive autoimmune arthritis via T helper 17 cells

    doi: 10.1016/j.immuni.2010.06.001

    Figure Lengend Snippet: Linking gut and spleen IL-17 cells (A) SI-LP lymphocytes were isolated from SPF or GF K/BxN mice. Cells were stained, analyzed by flow cytometry and gated as indicated. Expression of IL-17 versus CCR6 is plotted. The values indicate percentages of IL-17 + CCR6 + cells in CD3 + CD4 + B220 − cells. Data are representative of three independent experiments. (B) SI-LP lymphocytes (i) and splenocytes (ii) were isolated from SPF mice of the indicated ages, stained and analyzed by flow cytometry, gated as indicated. Plots displayed IL-17 versus CCR6 expression. Values indicate % of IL-17 + CCR6 + cells in total CD4 + T cells (CD3 + CD4 + B220 − ). Data are representative of two independent experiments. (iii) Measurement of ankle thickening for the same mice. Each circle represents one animal from two independent experiments. (C) Splenocytes from SPF BxN or K/BxN mice were stained and analyzed by flow cytometry, gated as indicated. Plots depict IL-17 versus α4β7 staining. Values indicate % of IL-17 + α4β7 + or IL-17 + α4β7 − cells in total CD4 + T cells (CD3 + CD4 + B220 − ). Data are representative of two independent experiments.

    Article Snippet: For IL-17A, a 10 μl final reaction mix containing TaqMan Universal PCR Master Mix (Applied Biosystems) and IL-17A TaqMan Gene Expression Assays (Mm00439619_m1) were used.

    Techniques: Isolation, Mouse Assay, Staining, Flow Cytometry, Cytometry, Expressing

    A defective Th17 signature in GF K/BxN mice ), using 2 as the cut-off for FC over the expression value of two other cell types. The volcano plots depict the FC for SPF vs GF K/BxN CD4 + T cells versus the p value of the FC. Signature genes are superimposed in red. Values refer to the number of genes upregulated (right) or downregulated (left) in GF vis-à-vis SPF T cells. P values from a X 2 test are indicated. (C) IL-4, IFN-γ and IL-17 transcripts in splenic CD4 + T cells for GF or SPF of B/N or K/BxN mice were quantified by RT-PCR. The level in SPF BxN mice was set as 1. Mean + s.e. Results were compiled from three independent experiments with two mice per group. P =0.01 for transcriptional fold-induction of IL-17 (SPF vs. GF K/BxN). (D) Splenocytes of GF or SPF BxN or K/BxN mice were stained with Abs recognizing CCR6 and IL-17, and were analyzed by flow cytometry. Values represent percentages of IL-17 + CCR6 + cells in CD3 + CD4 + B220 − cells. Data are representative of two independent experiments.

    Journal: Immunity

    Article Title: Gut-residing segmented filamentous bacteria drive autoimmune arthritis via T helper 17 cells

    doi: 10.1016/j.immuni.2010.06.001

    Figure Lengend Snippet: A defective Th17 signature in GF K/BxN mice ), using 2 as the cut-off for FC over the expression value of two other cell types. The volcano plots depict the FC for SPF vs GF K/BxN CD4 + T cells versus the p value of the FC. Signature genes are superimposed in red. Values refer to the number of genes upregulated (right) or downregulated (left) in GF vis-à-vis SPF T cells. P values from a X 2 test are indicated. (C) IL-4, IFN-γ and IL-17 transcripts in splenic CD4 + T cells for GF or SPF of B/N or K/BxN mice were quantified by RT-PCR. The level in SPF BxN mice was set as 1. Mean + s.e. Results were compiled from three independent experiments with two mice per group. P =0.01 for transcriptional fold-induction of IL-17 (SPF vs. GF K/BxN). (D) Splenocytes of GF or SPF BxN or K/BxN mice were stained with Abs recognizing CCR6 and IL-17, and were analyzed by flow cytometry. Values represent percentages of IL-17 + CCR6 + cells in CD3 + CD4 + B220 − cells. Data are representative of two independent experiments.

    Article Snippet: For IL-17A, a 10 μl final reaction mix containing TaqMan Universal PCR Master Mix (Applied Biosystems) and IL-17A TaqMan Gene Expression Assays (Mm00439619_m1) were used.

    Techniques: Mouse Assay, Expressing, Reverse Transcription Polymerase Chain Reaction, Staining, Flow Cytometry, Cytometry

    Reduction of arthritis by neutralization of IL-17 (A) 25-day-old SPF K/BxN mice were treated with 100μg of anti-IL-17 or control rat IgG every 3 days, and ankle thickening was measured over time (left panel). Mean ± s.e of the two groups (n=5 in both groups from two independent experiments is plotted; Asterisks indicate statistical significance using the Student s t-Test, *P

    Journal: Immunity

    Article Title: Gut-residing segmented filamentous bacteria drive autoimmune arthritis via T helper 17 cells

    doi: 10.1016/j.immuni.2010.06.001

    Figure Lengend Snippet: Reduction of arthritis by neutralization of IL-17 (A) 25-day-old SPF K/BxN mice were treated with 100μg of anti-IL-17 or control rat IgG every 3 days, and ankle thickening was measured over time (left panel). Mean ± s.e of the two groups (n=5 in both groups from two independent experiments is plotted; Asterisks indicate statistical significance using the Student s t-Test, *P

    Article Snippet: For IL-17A, a 10 μl final reaction mix containing TaqMan Universal PCR Master Mix (Applied Biosystems) and IL-17A TaqMan Gene Expression Assays (Mm00439619_m1) were used.

    Techniques: Neutralization, Mouse Assay

    Effects of various antibiotics (A) Representative dot plots examining expression of IL-17 and CCR6 by SI-LP lymphocytes in untreated or the indicated antibiotic-treated SPF K/BxN mice, treated from birth to 5 wks of age. Values refer to % of the gated population in total CD4 + T cells. Representative of two independent experiments. (B) SPF K/BxN mice were treated with metronidazole (1g/l), neomycin (1g/l), vancomycin (0.5g/l) or ampicillin (1g/l) in the drinking water from birth. At 5 weeks of age, SI-LP lymphocytes (left) and splenocytes (right) were isolated, stained and analyzed by flow cytometry. Plotted are the % of IL-17 + cells of total CD4 + T cells. Mean + s.e. (data was a combination of two independent experiments with mice treated with metronidazole (n=4), neomycin (n=4), vacomycin (n=4), ampicillin (n=4) or nothing (n=8)) Asterisks indicate statistical significance using the Student s t-Test, **P

    Journal: Immunity

    Article Title: Gut-residing segmented filamentous bacteria drive autoimmune arthritis via T helper 17 cells

    doi: 10.1016/j.immuni.2010.06.001

    Figure Lengend Snippet: Effects of various antibiotics (A) Representative dot plots examining expression of IL-17 and CCR6 by SI-LP lymphocytes in untreated or the indicated antibiotic-treated SPF K/BxN mice, treated from birth to 5 wks of age. Values refer to % of the gated population in total CD4 + T cells. Representative of two independent experiments. (B) SPF K/BxN mice were treated with metronidazole (1g/l), neomycin (1g/l), vancomycin (0.5g/l) or ampicillin (1g/l) in the drinking water from birth. At 5 weeks of age, SI-LP lymphocytes (left) and splenocytes (right) were isolated, stained and analyzed by flow cytometry. Plotted are the % of IL-17 + cells of total CD4 + T cells. Mean + s.e. (data was a combination of two independent experiments with mice treated with metronidazole (n=4), neomycin (n=4), vacomycin (n=4), ampicillin (n=4) or nothing (n=8)) Asterisks indicate statistical significance using the Student s t-Test, **P

    Article Snippet: For IL-17A, a 10 μl final reaction mix containing TaqMan Universal PCR Master Mix (Applied Biosystems) and IL-17A TaqMan Gene Expression Assays (Mm00439619_m1) were used.

    Techniques: Expressing, Mouse Assay, Isolation, Staining, Flow Cytometry, Cytometry