antibodies against il 27  (Thermo Fisher)


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    anti IL 27
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    Structured Review

    Thermo Fisher antibodies against il 27
    Mice lacking <t>IL-27/WSX-1</t> signalling still develop mechanical hypersensitivity after inflammation and peripheral nerve injury. Mice were subjected to the ( a – c) inflammatory or ( d – g ) neuropathic pain model. Fifty percent paw withdrawal threshold before and after ( a ) CFA injection or ( d ) spinal nerve injury. ( b , e ) The percent change in paw withdrawal threshold calculated from a and d, respectively. Each value after CFA injection or nerve injury was normalised by the control value (pre) in each mouse. ( c ) Hind paw weight, as a measure of oedema, in mice 14 days after i.pl. CFA injection. ( f ) Representative immunofluorescence labelling for Iba1 (green) with nuclear staining with TO-PRO-3 (blue) in a transverse section of the dorsal horns from the L4 segment of WT, WSX-1 −/− , EBI3 −/− , and p28 −/− mice 7 days after spinal nerve injury. ( g ) Number of Iba1-positive cells in the ipsilateral or contralateral dorsal horn of L4 spinal segments dissected from WT, WSX-1 −/− , EBI3 −/− , and p28 −/− mice 7 days after spinal nerve injury. n = 5 animals/group. All data are expressed as means ± SEM.

    https://www.bioz.com/result/antibodies against il 27/product/Thermo Fisher
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    antibodies against il 27 - by Bioz Stars, 2021-07
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    1) Product Images from "Interleukin-27 controls basal pain threshold in physiological and pathological conditions"

    Article Title: Interleukin-27 controls basal pain threshold in physiological and pathological conditions

    Journal: Scientific Reports

    doi: 10.1038/s41598-018-29398-3

    Mice lacking IL-27/WSX-1 signalling still develop mechanical hypersensitivity after inflammation and peripheral nerve injury. Mice were subjected to the ( a – c) inflammatory or ( d – g ) neuropathic pain model. Fifty percent paw withdrawal threshold before and after ( a ) CFA injection or ( d ) spinal nerve injury. ( b , e ) The percent change in paw withdrawal threshold calculated from a and d, respectively. Each value after CFA injection or nerve injury was normalised by the control value (pre) in each mouse. ( c ) Hind paw weight, as a measure of oedema, in mice 14 days after i.pl. CFA injection. ( f ) Representative immunofluorescence labelling for Iba1 (green) with nuclear staining with TO-PRO-3 (blue) in a transverse section of the dorsal horns from the L4 segment of WT, WSX-1 −/− , EBI3 −/− , and p28 −/− mice 7 days after spinal nerve injury. ( g ) Number of Iba1-positive cells in the ipsilateral or contralateral dorsal horn of L4 spinal segments dissected from WT, WSX-1 −/− , EBI3 −/− , and p28 −/− mice 7 days after spinal nerve injury. n = 5 animals/group. All data are expressed as means ± SEM.
    Figure Legend Snippet: Mice lacking IL-27/WSX-1 signalling still develop mechanical hypersensitivity after inflammation and peripheral nerve injury. Mice were subjected to the ( a – c) inflammatory or ( d – g ) neuropathic pain model. Fifty percent paw withdrawal threshold before and after ( a ) CFA injection or ( d ) spinal nerve injury. ( b , e ) The percent change in paw withdrawal threshold calculated from a and d, respectively. Each value after CFA injection or nerve injury was normalised by the control value (pre) in each mouse. ( c ) Hind paw weight, as a measure of oedema, in mice 14 days after i.pl. CFA injection. ( f ) Representative immunofluorescence labelling for Iba1 (green) with nuclear staining with TO-PRO-3 (blue) in a transverse section of the dorsal horns from the L4 segment of WT, WSX-1 −/− , EBI3 −/− , and p28 −/− mice 7 days after spinal nerve injury. ( g ) Number of Iba1-positive cells in the ipsilateral or contralateral dorsal horn of L4 spinal segments dissected from WT, WSX-1 −/− , EBI3 −/− , and p28 −/− mice 7 days after spinal nerve injury. n = 5 animals/group. All data are expressed as means ± SEM.

    Techniques Used: Mouse Assay, Injection, Immunofluorescence, Staining

    Facilitated mechanical sensitivity of C-fibre nociceptors in mice lacking IL-27/WSX-1 signalling. ( a ) Sample recordings of peri-stimulus time histogram. Abscissa: time in seconds. Ordinate: discharge rate of C-nociceptors. Lowest trace: force output of the mechanical stimulus. ( b ) Summarised mechanical response patterns. The response magnitude was significantly greater in WSX-1 −/− , EBI3 −/− , and p28 −/− mice compared with WT. ( a , b ) WT (n = 28), WSX-1 −/− (n = 29), EBI3 −/− (n = 25), p28 −/− (n = 19). P
    Figure Legend Snippet: Facilitated mechanical sensitivity of C-fibre nociceptors in mice lacking IL-27/WSX-1 signalling. ( a ) Sample recordings of peri-stimulus time histogram. Abscissa: time in seconds. Ordinate: discharge rate of C-nociceptors. Lowest trace: force output of the mechanical stimulus. ( b ) Summarised mechanical response patterns. The response magnitude was significantly greater in WSX-1 −/− , EBI3 −/− , and p28 −/− mice compared with WT. ( a , b ) WT (n = 28), WSX-1 −/− (n = 29), EBI3 −/− (n = 25), p28 −/− (n = 19). P

    Techniques Used: Mouse Assay

    Lack of IL-27/WSX-1 signalling results in enhanced nociceptive behaviours. Reaction latencies to heat measured with the ( a ) hot-plate and ( b ) tail-flick tests. ( c ) Acetone test, in which values represent reaction scores after acetone application to a hind paw. ( d ) Fifty percent paw withdrawal threshold measured with the von Frey test. ( e ) Duration of licking and biting during the first (0–10 min) and second (10–60 min) phases after formalin injection into a hind paw. ( f ) Duration of licking and biting after capsaicin injection into a hind paw. n = 5–10. * P
    Figure Legend Snippet: Lack of IL-27/WSX-1 signalling results in enhanced nociceptive behaviours. Reaction latencies to heat measured with the ( a ) hot-plate and ( b ) tail-flick tests. ( c ) Acetone test, in which values represent reaction scores after acetone application to a hind paw. ( d ) Fifty percent paw withdrawal threshold measured with the von Frey test. ( e ) Duration of licking and biting during the first (0–10 min) and second (10–60 min) phases after formalin injection into a hind paw. ( f ) Duration of licking and biting after capsaicin injection into a hind paw. n = 5–10. * P

    Techniques Used: Tail Flick Test, Injection

    Intraplantar blockade of IL-27 decreased paw withdrawal threshold in naïve WT mice. Fifty percent paw withdrawal threshold before and after i.pl. injection of a neutralising antibody against p28 or control IgG into WT mice. n = 3–5 animals/group. * P
    Figure Legend Snippet: Intraplantar blockade of IL-27 decreased paw withdrawal threshold in naïve WT mice. Fifty percent paw withdrawal threshold before and after i.pl. injection of a neutralising antibody against p28 or control IgG into WT mice. n = 3–5 animals/group. * P

    Techniques Used: Mouse Assay, Injection

    IL-27 is an endogenous regulator of thermal and mechanical nociceptive responses. ( a ) Single i.p. injection of rIL-27 dose-dependently prolonged hot-plate latency in EBI3 −/− mice. ( b ) Quick restoration of hot-plate latencies in p28 −/− , but not WSX-1 −/− and WT mice following a single i.p. injection of rIL-27 (16 µg/kg). ( c ) A single i.p. injection of rIL-27 (16 µg/kg) also significantly alleviated mechanical hypersensitivity in EBI3 −/− mice. ( d ) A single i.p. injection of neutralising antibody against p28 (1.6 mg/kg) decreased the paw withdrawal threshold in naïve WT mice. n = 5 animals/group. * P
    Figure Legend Snippet: IL-27 is an endogenous regulator of thermal and mechanical nociceptive responses. ( a ) Single i.p. injection of rIL-27 dose-dependently prolonged hot-plate latency in EBI3 −/− mice. ( b ) Quick restoration of hot-plate latencies in p28 −/− , but not WSX-1 −/− and WT mice following a single i.p. injection of rIL-27 (16 µg/kg). ( c ) A single i.p. injection of rIL-27 (16 µg/kg) also significantly alleviated mechanical hypersensitivity in EBI3 −/− mice. ( d ) A single i.p. injection of neutralising antibody against p28 (1.6 mg/kg) decreased the paw withdrawal threshold in naïve WT mice. n = 5 animals/group. * P

    Techniques Used: Injection, Mouse Assay

    2) Product Images from "Interleukin-27 controls basal pain threshold in physiological and pathological conditions"

    Article Title: Interleukin-27 controls basal pain threshold in physiological and pathological conditions

    Journal: Scientific Reports

    doi: 10.1038/s41598-018-29398-3

    Mice lacking IL-27/WSX-1 signalling still develop mechanical hypersensitivity after inflammation and peripheral nerve injury. Mice were subjected to the ( a – c) inflammatory or ( d – g ) neuropathic pain model. Fifty percent paw withdrawal threshold before and after ( a ) CFA injection or ( d ) spinal nerve injury. ( b , e ) The percent change in paw withdrawal threshold calculated from a and d, respectively. Each value after CFA injection or nerve injury was normalised by the control value (pre) in each mouse. ( c ) Hind paw weight, as a measure of oedema, in mice 14 days after i.pl. CFA injection. ( f ) Representative immunofluorescence labelling for Iba1 (green) with nuclear staining with TO-PRO-3 (blue) in a transverse section of the dorsal horns from the L4 segment of WT, WSX-1 −/− , EBI3 −/− , and p28 −/− mice 7 days after spinal nerve injury. ( g ) Number of Iba1-positive cells in the ipsilateral or contralateral dorsal horn of L4 spinal segments dissected from WT, WSX-1 −/− , EBI3 −/− , and p28 −/− mice 7 days after spinal nerve injury. n = 5 animals/group. All data are expressed as means ± SEM.
    Figure Legend Snippet: Mice lacking IL-27/WSX-1 signalling still develop mechanical hypersensitivity after inflammation and peripheral nerve injury. Mice were subjected to the ( a – c) inflammatory or ( d – g ) neuropathic pain model. Fifty percent paw withdrawal threshold before and after ( a ) CFA injection or ( d ) spinal nerve injury. ( b , e ) The percent change in paw withdrawal threshold calculated from a and d, respectively. Each value after CFA injection or nerve injury was normalised by the control value (pre) in each mouse. ( c ) Hind paw weight, as a measure of oedema, in mice 14 days after i.pl. CFA injection. ( f ) Representative immunofluorescence labelling for Iba1 (green) with nuclear staining with TO-PRO-3 (blue) in a transverse section of the dorsal horns from the L4 segment of WT, WSX-1 −/− , EBI3 −/− , and p28 −/− mice 7 days after spinal nerve injury. ( g ) Number of Iba1-positive cells in the ipsilateral or contralateral dorsal horn of L4 spinal segments dissected from WT, WSX-1 −/− , EBI3 −/− , and p28 −/− mice 7 days after spinal nerve injury. n = 5 animals/group. All data are expressed as means ± SEM.

    Techniques Used: Mouse Assay, Injection, Immunofluorescence, Staining

    Facilitated mechanical sensitivity of C-fibre nociceptors in mice lacking IL-27/WSX-1 signalling. ( a ) Sample recordings of peri-stimulus time histogram. Abscissa: time in seconds. Ordinate: discharge rate of C-nociceptors. Lowest trace: force output of the mechanical stimulus. ( b ) Summarised mechanical response patterns. The response magnitude was significantly greater in WSX-1 −/− , EBI3 −/− , and p28 −/− mice compared with WT. ( a , b ) WT (n = 28), WSX-1 −/− (n = 29), EBI3 −/− (n = 25), p28 −/− (n = 19). P
    Figure Legend Snippet: Facilitated mechanical sensitivity of C-fibre nociceptors in mice lacking IL-27/WSX-1 signalling. ( a ) Sample recordings of peri-stimulus time histogram. Abscissa: time in seconds. Ordinate: discharge rate of C-nociceptors. Lowest trace: force output of the mechanical stimulus. ( b ) Summarised mechanical response patterns. The response magnitude was significantly greater in WSX-1 −/− , EBI3 −/− , and p28 −/− mice compared with WT. ( a , b ) WT (n = 28), WSX-1 −/− (n = 29), EBI3 −/− (n = 25), p28 −/− (n = 19). P

    Techniques Used: Mouse Assay

    Lack of IL-27/WSX-1 signalling results in enhanced nociceptive behaviours. Reaction latencies to heat measured with the ( a ) hot-plate and ( b ) tail-flick tests. ( c ) Acetone test, in which values represent reaction scores after acetone application to a hind paw. ( d ) Fifty percent paw withdrawal threshold measured with the von Frey test. ( e ) Duration of licking and biting during the first (0–10 min) and second (10–60 min) phases after formalin injection into a hind paw. ( f ) Duration of licking and biting after capsaicin injection into a hind paw. n = 5–10. * P
    Figure Legend Snippet: Lack of IL-27/WSX-1 signalling results in enhanced nociceptive behaviours. Reaction latencies to heat measured with the ( a ) hot-plate and ( b ) tail-flick tests. ( c ) Acetone test, in which values represent reaction scores after acetone application to a hind paw. ( d ) Fifty percent paw withdrawal threshold measured with the von Frey test. ( e ) Duration of licking and biting during the first (0–10 min) and second (10–60 min) phases after formalin injection into a hind paw. ( f ) Duration of licking and biting after capsaicin injection into a hind paw. n = 5–10. * P

    Techniques Used: Tail Flick Test, Injection

    Intraplantar blockade of IL-27 decreased paw withdrawal threshold in naïve WT mice. Fifty percent paw withdrawal threshold before and after i.pl. injection of a neutralising antibody against p28 or control IgG into WT mice. n = 3–5 animals/group. * P
    Figure Legend Snippet: Intraplantar blockade of IL-27 decreased paw withdrawal threshold in naïve WT mice. Fifty percent paw withdrawal threshold before and after i.pl. injection of a neutralising antibody against p28 or control IgG into WT mice. n = 3–5 animals/group. * P

    Techniques Used: Mouse Assay, Injection

    IL-27 is an endogenous regulator of thermal and mechanical nociceptive responses. ( a ) Single i.p. injection of rIL-27 dose-dependently prolonged hot-plate latency in EBI3 −/− mice. ( b ) Quick restoration of hot-plate latencies in p28 −/− , but not WSX-1 −/− and WT mice following a single i.p. injection of rIL-27 (16 µg/kg). ( c ) A single i.p. injection of rIL-27 (16 µg/kg) also significantly alleviated mechanical hypersensitivity in EBI3 −/− mice. ( d ) A single i.p. injection of neutralising antibody against p28 (1.6 mg/kg) decreased the paw withdrawal threshold in naïve WT mice. n = 5 animals/group. * P
    Figure Legend Snippet: IL-27 is an endogenous regulator of thermal and mechanical nociceptive responses. ( a ) Single i.p. injection of rIL-27 dose-dependently prolonged hot-plate latency in EBI3 −/− mice. ( b ) Quick restoration of hot-plate latencies in p28 −/− , but not WSX-1 −/− and WT mice following a single i.p. injection of rIL-27 (16 µg/kg). ( c ) A single i.p. injection of rIL-27 (16 µg/kg) also significantly alleviated mechanical hypersensitivity in EBI3 −/− mice. ( d ) A single i.p. injection of neutralising antibody against p28 (1.6 mg/kg) decreased the paw withdrawal threshold in naïve WT mice. n = 5 animals/group. * P

    Techniques Used: Injection, Mouse Assay

    Related Articles

    Mouse Assay:

    Article Title: Interleukin-27 controls basal pain threshold in physiological and pathological conditions
    Article Snippet: In another set of experiments, EBI3 −/− mice received an i.p. injection of rIL-27 (16 µg/kg) or saline to assess the effects on mechanical sensitivity by using the von Frey test. .. To test whether neutralising antibodies against IL-27 could mimic phenotypes observed in mice lacking IL-27/WSX-1 signalling, WT mice received an i.p. or i.pl. injection of anti-mouse IL-27 (p28) neutralising antibody (1.6 mg/kg or 16 µg/kg, respectively, mouse IgG2a κ isotype, Affymetrix, Santa Clara, CA) or the same dose of an isotype-matched control antibody (mouse IgG2a κ isotype, Affymetrix). ..

    Injection:

    Article Title: Interleukin-27 controls basal pain threshold in physiological and pathological conditions
    Article Snippet: In another set of experiments, EBI3 −/− mice received an i.p. injection of rIL-27 (16 µg/kg) or saline to assess the effects on mechanical sensitivity by using the von Frey test. .. To test whether neutralising antibodies against IL-27 could mimic phenotypes observed in mice lacking IL-27/WSX-1 signalling, WT mice received an i.p. or i.pl. injection of anti-mouse IL-27 (p28) neutralising antibody (1.6 mg/kg or 16 µg/kg, respectively, mouse IgG2a κ isotype, Affymetrix, Santa Clara, CA) or the same dose of an isotype-matched control antibody (mouse IgG2a κ isotype, Affymetrix). ..

    Immunofluorescence:

    Article Title: IL-27 suppresses antimicrobial activity in human leprosy
    Article Snippet: Two- and three-color immunofluorescence with confocal microscopy was used to colocalize cytokines with specific cell markers. .. Immunofluorescence was performed by serially incubating cryostat tissue sections with mouse anti-human mAbs of different isotypes, anti-CD3 (Clone: UCHT1; IgG1), anti-CD163 (Clone: GH1/61; IgG1), anti-CD209 (Clone: DCN46; IgG2b), anti-IFN-β (Clone: MMHB-3; IgG1 or Clone: MMHB-1; IgG2a), anti-IL-10 (Clone: 127107; IgG1 directly conjugated to PE) and anti-IL-27 (Clone: 307426;IgG2a) followed by incubation with isotype-specific, fluorochrome (A488, A568 or A647)-labeled goat anti-mouse immunoglobulin antibodies (Molecular Probes, Carlsbad, CA). .. Controls included staining with isotype-matched antibodies as described previously ( ).

    Incubation:

    Article Title: IL-27 suppresses antimicrobial activity in human leprosy
    Article Snippet: Two- and three-color immunofluorescence with confocal microscopy was used to colocalize cytokines with specific cell markers. .. Immunofluorescence was performed by serially incubating cryostat tissue sections with mouse anti-human mAbs of different isotypes, anti-CD3 (Clone: UCHT1; IgG1), anti-CD163 (Clone: GH1/61; IgG1), anti-CD209 (Clone: DCN46; IgG2b), anti-IFN-β (Clone: MMHB-3; IgG1 or Clone: MMHB-1; IgG2a), anti-IL-10 (Clone: 127107; IgG1 directly conjugated to PE) and anti-IL-27 (Clone: 307426;IgG2a) followed by incubation with isotype-specific, fluorochrome (A488, A568 or A647)-labeled goat anti-mouse immunoglobulin antibodies (Molecular Probes, Carlsbad, CA). .. Controls included staining with isotype-matched antibodies as described previously ( ).

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    Thermo Fisher fluorochrome conjugated antibodies against il 17a
    γδ T cells are the primary source of IL-17 during S. aureus induced peritonitis Mice were infected with S. aureus (5×10 8 CFU) via i.p. injection. At the indicated times post–infection, the peritoneal cavity was lavaged and the MLN collected. Secreted <t>IL-17A</t> and IL-1β in the peritoneal fluid was measured by ELISA (A). 3 h post-infection (B, C), and at the indicated time-points (D E), PECs (B D) and MLN cells (C E), cultured with Brefeldin A but not PMA and ionomycin, were stained for surface CD3, CD4, CD8 and γδTCR, and intracellular IL-17, and analysed by flow cytometry. IL-1RI −/− and WT mice were infected with S. aureus (5×10 8 CFU) via i.p. injection and at 3 h post-infection PECs, cultured with Brefeldin A but not PMA and ionomycin, were stained for surface CD3 and γδTCR, and intracellular IL-17, and analysed by flow cytometry (F). Results expressed as mean ± SEM of n=10 mice/ group, with representative FACS plots. *
    Fluorochrome Conjugated Antibodies Against Il 17a, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/fluorochrome conjugated antibodies against il 17a/product/Thermo Fisher
    Average 94 stars, based on 1 article reviews
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    γδ T cells are the primary source of IL-17 during S. aureus induced peritonitis Mice were infected with S. aureus (5×10 8 CFU) via i.p. injection. At the indicated times post–infection, the peritoneal cavity was lavaged and the MLN collected. Secreted IL-17A and IL-1β in the peritoneal fluid was measured by ELISA (A). 3 h post-infection (B, C), and at the indicated time-points (D E), PECs (B D) and MLN cells (C E), cultured with Brefeldin A but not PMA and ionomycin, were stained for surface CD3, CD4, CD8 and γδTCR, and intracellular IL-17, and analysed by flow cytometry. IL-1RI −/− and WT mice were infected with S. aureus (5×10 8 CFU) via i.p. injection and at 3 h post-infection PECs, cultured with Brefeldin A but not PMA and ionomycin, were stained for surface CD3 and γδTCR, and intracellular IL-17, and analysed by flow cytometry (F). Results expressed as mean ± SEM of n=10 mice/ group, with representative FACS plots. *

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

    Article Title: Staphylococcus aureus infection of mice expands a population of memory γδ T cells that are protective against subsequent infection

    doi: 10.4049/jimmunol.1303420

    Figure Lengend Snippet: γδ T cells are the primary source of IL-17 during S. aureus induced peritonitis Mice were infected with S. aureus (5×10 8 CFU) via i.p. injection. At the indicated times post–infection, the peritoneal cavity was lavaged and the MLN collected. Secreted IL-17A and IL-1β in the peritoneal fluid was measured by ELISA (A). 3 h post-infection (B, C), and at the indicated time-points (D E), PECs (B D) and MLN cells (C E), cultured with Brefeldin A but not PMA and ionomycin, were stained for surface CD3, CD4, CD8 and γδTCR, and intracellular IL-17, and analysed by flow cytometry. IL-1RI −/− and WT mice were infected with S. aureus (5×10 8 CFU) via i.p. injection and at 3 h post-infection PECs, cultured with Brefeldin A but not PMA and ionomycin, were stained for surface CD3 and γδTCR, and intracellular IL-17, and analysed by flow cytometry (F). Results expressed as mean ± SEM of n=10 mice/ group, with representative FACS plots. *

    Article Snippet: Cells were fixed and permeabilised using the Dako cytomation Intrastain Kit, before intracellular staining with a fluorochrome-conjugated antibodies against IL-17A (eBioscience, clone 17B7) and IFNγ (eBioscience, clone XMG1.2).

    Techniques: Mouse Assay, Infection, Injection, Enzyme-linked Immunosorbent Assay, Cell Culture, Staining, Flow Cytometry, Cytometry, FACS

    Sulforaphene administration promotesIL-17 + γδT cells in cLP of colitis mice. (A) The IL-17A protein concentration in each animal group was detected in supernatants of colonic tissue homogenates by ELISA. (B) Representative flow cytometry plots of CD4 + T cells identified using side scatter (SSC) and forward scatter (FSC) plots (left panel) and TCR-γδ + expression. Representative flow cytometry plots of Th17 cells (CD4 + IL-17 + ) and γδT17 cells (TCR-γδ + IL-17 + )in the LP of mouse colon (right panel). (C) . Percentage of γδT17 cells in γδT cells of cLP in mice ( n = 7 mice per group). (D) Percentage of Th17 cells in CD4 + T cells of cLP in mice ( n = 7). (E) The relative expression levels of il17a and RORγt in colon tissues of mice detected by quantitative real-time PCR (qPCR). (F) Quantification of TLR2 expressing γδT cells (TLR2 + TCR-γδ + ) in the cLP of mice in different groups. (G) Representative flow cytometry analysis of TLR2 expressing γδT cells. Error bars represent mean ± SEM ( n = 7). Statistical analysis of the quantitative multiple group comparisons was performed using the one-way analysis of variance (ANOVA) followed by Tukey’s test, ∗ p

    Journal: Frontiers in Pharmacology

    Article Title: Traditional Herbal Medicine-Derived Sulforaphene LFS-01 Reverses Colitis in Mice by Selectively Altering the Gut Microbiota and Promoting Intestinal Gamma-Delta T Cells

    doi: 10.3389/fphar.2017.00959

    Figure Lengend Snippet: Sulforaphene administration promotesIL-17 + γδT cells in cLP of colitis mice. (A) The IL-17A protein concentration in each animal group was detected in supernatants of colonic tissue homogenates by ELISA. (B) Representative flow cytometry plots of CD4 + T cells identified using side scatter (SSC) and forward scatter (FSC) plots (left panel) and TCR-γδ + expression. Representative flow cytometry plots of Th17 cells (CD4 + IL-17 + ) and γδT17 cells (TCR-γδ + IL-17 + )in the LP of mouse colon (right panel). (C) . Percentage of γδT17 cells in γδT cells of cLP in mice ( n = 7 mice per group). (D) Percentage of Th17 cells in CD4 + T cells of cLP in mice ( n = 7). (E) The relative expression levels of il17a and RORγt in colon tissues of mice detected by quantitative real-time PCR (qPCR). (F) Quantification of TLR2 expressing γδT cells (TLR2 + TCR-γδ + ) in the cLP of mice in different groups. (G) Representative flow cytometry analysis of TLR2 expressing γδT cells. Error bars represent mean ± SEM ( n = 7). Statistical analysis of the quantitative multiple group comparisons was performed using the one-way analysis of variance (ANOVA) followed by Tukey’s test, ∗ p

    Article Snippet: Cells were then fixed and permeabilized with cytofix-cytoperm kit (BD) followed by intracellular staining using antibodies against IL-17A (Anti-Mouse /Rat IL-17A APC, 17-7177, eBioscience).

    Techniques: Mouse Assay, Protein Concentration, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Cytometry, Expressing, Real-time Polymerase Chain Reaction

    Ahr Deficiency in IEC Impairs Resistance to Citrobacter rodentium (A) Survival plot of bone marrow chimeras infected with C. rodentium (WT→ WT; Ahr −/− → WT; Ahr −/− → Ahr −/− ; WT → Ahr −/− ); n = 5 per group. (B) Absolute numbers of colonic RORγt + ILC3 and IL-17A-producing TCRβ + CD4 + T cells (WT, n = 7; Villin Cre Ahr fl/fl , n = 7) at day 7. (C) IL-22 protein content in colon explant cultures (WT, n = 12; Villin Cre Ahr fl/fl , n = 12). Data represent pooled results of at least two independent experiments. (D) qPCR analysis of antimicrobial ( IL-22 , Reg3g , S100a9 ) in colon from WT and Villin Cre Ahr fl/fl mice at day 7. (E) C. rodentium burdens in colon, liver, and spleen. Bars show the median and each symbol represents an individual mouse. (F) Colon sections stained for E-cadherin (green), C. rodentium (red), and DAPI (blue). Scale bars, 50 μm. (G) Survival plot of mice infected with C. rodentium (WT, n = 7; Villin Cre Ahr fl/fl , n = 7). (H) qPCR analysis of the goblet cell marker Muc2 and enterocyte marker Car4 (WT, n = 7; Villin Cre Ahr fl/fl , n = 7). (I) Representative image of AB-PAS staining in WT and Villin Cre Ahr fl/fl . Scale bars, 50 μm. (J) Quantification of the number of AB-PAS-positive cells per 20 crypts in WT and Villin Cre Ahr fl/fl . Error bars, mean + SEM. ∗ p

    Journal: Immunity

    Article Title: The Environmental Sensor AHR Protects from Inflammatory Damage by Maintaining Intestinal Stem Cell Homeostasis and Barrier Integrity

    doi: 10.1016/j.immuni.2018.07.010

    Figure Lengend Snippet: Ahr Deficiency in IEC Impairs Resistance to Citrobacter rodentium (A) Survival plot of bone marrow chimeras infected with C. rodentium (WT→ WT; Ahr −/− → WT; Ahr −/− → Ahr −/− ; WT → Ahr −/− ); n = 5 per group. (B) Absolute numbers of colonic RORγt + ILC3 and IL-17A-producing TCRβ + CD4 + T cells (WT, n = 7; Villin Cre Ahr fl/fl , n = 7) at day 7. (C) IL-22 protein content in colon explant cultures (WT, n = 12; Villin Cre Ahr fl/fl , n = 12). Data represent pooled results of at least two independent experiments. (D) qPCR analysis of antimicrobial ( IL-22 , Reg3g , S100a9 ) in colon from WT and Villin Cre Ahr fl/fl mice at day 7. (E) C. rodentium burdens in colon, liver, and spleen. Bars show the median and each symbol represents an individual mouse. (F) Colon sections stained for E-cadherin (green), C. rodentium (red), and DAPI (blue). Scale bars, 50 μm. (G) Survival plot of mice infected with C. rodentium (WT, n = 7; Villin Cre Ahr fl/fl , n = 7). (H) qPCR analysis of the goblet cell marker Muc2 and enterocyte marker Car4 (WT, n = 7; Villin Cre Ahr fl/fl , n = 7). (I) Representative image of AB-PAS staining in WT and Villin Cre Ahr fl/fl . Scale bars, 50 μm. (J) Quantification of the number of AB-PAS-positive cells per 20 crypts in WT and Villin Cre Ahr fl/fl . Error bars, mean + SEM. ∗ p

    Article Snippet: Cell were then fixed in eBioscience Fix/Perm buffer or 4% formaldehyde (for preservation of eYFP fluorescence) for 30min on ice followed by permeabilization in eBioscience permeabilization buffer for 45min in the presence of antibodies against IL-17A, IL-22, (all ebioscience) and RORγt (BD Biosciences).

    Techniques: Infection, Real-time Polymerase Chain Reaction, Mouse Assay, Staining, Marker

    Human S . aureus bloodstream infection is associated with increased IFNγ production. Serum from S . aureus and E . coli bloodstream infection patients was collected on day 7 ± 2 post-initial bacteraemia and assessed for IFNγ (A) and IL-17A (B) by ELISA. Results expressed as individual patient values with median indicated by bar, n = 11–24 per group. *p

    Journal: PLoS Pathogens

    Article Title: Memory Th1 Cells Are Protective in Invasive Staphylococcus aureus Infection

    doi: 10.1371/journal.ppat.1005226

    Figure Lengend Snippet: Human S . aureus bloodstream infection is associated with increased IFNγ production. Serum from S . aureus and E . coli bloodstream infection patients was collected on day 7 ± 2 post-initial bacteraemia and assessed for IFNγ (A) and IL-17A (B) by ELISA. Results expressed as individual patient values with median indicated by bar, n = 11–24 per group. *p

    Article Snippet: Cells were fixed and permeabilised using the Dako IntraStain Fixation and Permeabilization Kit, followed by intracellular staining with fluorochrome-conjugated antibodies against IL-17A (eBioscience, clone eBio64DEC17) and IFNγ (eBioscience, clone 4S.B3).

    Techniques: Infection, Enzyme-linked Immunosorbent Assay

    Human S . aureus bloodstream infection induces S . aureus antigen-specific Th1 cells. PBMCs were isolated from patients, CFSE-labelled and incubated with heat-killed S . aureus PS80 strain (1μg/ml ≈ 1x10 7 CFU/ml) or media alone for 10 d before assessing S . aureus antigen-specific proliferation by gating on CFSE lo cells of the CD4 + population using flow cytometry (A). S . aureus antigen-specific Th1 and cytotoxic T cell division was assessed by gating on CFSE lo IFNγ + cells of the CD4 + and CD8 + populations respectively (B). S . aureus antigen-specific Th1 and Th17 proportions were compared by gating on CFSE lo IFNγ + or IL-17A + cells in the CD4 + population (C). For each patient, media only responses were subtracted from responses to heat-killed S . aureus to determine the antigen-specific response. Results shown as box-and-whiskers plots where the horizontal line indicates the median, boundaries of the box indicate the IQR, and whiskers indicate the highest and lowest values of the results, and representative FACS plots of CD4 + or CD8 + lymphocytes (A, B). n = 5–17 per group. SA = S . aureus , EC = E . coli , BSI = bloodstream infection. *p

    Journal: PLoS Pathogens

    Article Title: Memory Th1 Cells Are Protective in Invasive Staphylococcus aureus Infection

    doi: 10.1371/journal.ppat.1005226

    Figure Lengend Snippet: Human S . aureus bloodstream infection induces S . aureus antigen-specific Th1 cells. PBMCs were isolated from patients, CFSE-labelled and incubated with heat-killed S . aureus PS80 strain (1μg/ml ≈ 1x10 7 CFU/ml) or media alone for 10 d before assessing S . aureus antigen-specific proliferation by gating on CFSE lo cells of the CD4 + population using flow cytometry (A). S . aureus antigen-specific Th1 and cytotoxic T cell division was assessed by gating on CFSE lo IFNγ + cells of the CD4 + and CD8 + populations respectively (B). S . aureus antigen-specific Th1 and Th17 proportions were compared by gating on CFSE lo IFNγ + or IL-17A + cells in the CD4 + population (C). For each patient, media only responses were subtracted from responses to heat-killed S . aureus to determine the antigen-specific response. Results shown as box-and-whiskers plots where the horizontal line indicates the median, boundaries of the box indicate the IQR, and whiskers indicate the highest and lowest values of the results, and representative FACS plots of CD4 + or CD8 + lymphocytes (A, B). n = 5–17 per group. SA = S . aureus , EC = E . coli , BSI = bloodstream infection. *p

    Article Snippet: Cells were fixed and permeabilised using the Dako IntraStain Fixation and Permeabilization Kit, followed by intracellular staining with fluorochrome-conjugated antibodies against IL-17A (eBioscience, clone eBio64DEC17) and IFNγ (eBioscience, clone 4S.B3).

    Techniques: Infection, Isolation, Incubation, Flow Cytometry, Cytometry, FACS