recombinant human il 17f protein cf  (R&D Systems)

 
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    Name:
    Recombinant Human IL 17F Protein
    Description:
    The Recombinant Human IL 17F Protein from R D Systems is derived from E coli The Recombinant Human IL 17F Protein has been validated for the following applications Bioactivity
    Catalog Number:
    1335-IL-025
    Price:
    329
    Category:
    Proteins and Enzymes
    Source:
    E. coli-derived Recombinant Human IL-17F Protein
    Applications:
    Bioactivity
    Purity:
    >97%, by SDS-PAGE under reducing conditions and visualized by silver stain
    Conjugate:
    Unconjugated
    Size:
    25 ug
    Buy from Supplier


    Structured Review

    R&D Systems recombinant human il 17f protein cf
    Reversal of Th17 suppressor resistance following neutralization of IL-17A, <t>IL-17F,</t> or IL-17AF cytokines or blockade of IL-17RA and/or IL-17RC on CD4+ T cells, but not on CD8+ T cells or APC. Naïve CD4+CD25- T cells obtained from healthy donor PBMCs were cultured in Th0 conditions ( A ) or under Th17 differentiation conditions ( B ). Differentiated Th subsets were CFSE-stained and incubated with various IL-17 cytokine neutralizing antibodies, as indicated, and then placed in suppression assays with autologous CD8+ T cells and irradiated APCs and fixed αCD3 for 7 d. ( C ). Th0 and Th17 cells were placed into routine CD8+ suppression assays as in prior figures (Th0 and Th17 controls). In parallel, Th17 cells, autologous APC, or CD8+ T cells were first incubated for 90 min with antibodies against IL-17RA, IL17-RC, or a combination of both. Cells were then washed and used in CD8+ suppression assays in a way that one of the cell types had been preincubated for receptor blockade. The bars indicate normalized suppression data (mean ± SEM), where the baseline suppression observed in the Th0 conditions was designated as 100%. * P
    The Recombinant Human IL 17F Protein from R D Systems is derived from E coli The Recombinant Human IL 17F Protein has been validated for the following applications Bioactivity
    https://www.bioz.com/result/recombinant human il 17f protein cf/product/R&D Systems
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    recombinant human il 17f protein cf - by Bioz Stars, 2021-07
    93/100 stars

    Images

    1) Product Images from "CD4 T cell-intrinsic role for the T helper 17 signature cytokine IL-17: Effector resistance to immune suppression"

    Article Title: CD4 T cell-intrinsic role for the T helper 17 signature cytokine IL-17: Effector resistance to immune suppression

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

    doi: 10.1073/pnas.2005010117

    Reversal of Th17 suppressor resistance following neutralization of IL-17A, IL-17F, or IL-17AF cytokines or blockade of IL-17RA and/or IL-17RC on CD4+ T cells, but not on CD8+ T cells or APC. Naïve CD4+CD25- T cells obtained from healthy donor PBMCs were cultured in Th0 conditions ( A ) or under Th17 differentiation conditions ( B ). Differentiated Th subsets were CFSE-stained and incubated with various IL-17 cytokine neutralizing antibodies, as indicated, and then placed in suppression assays with autologous CD8+ T cells and irradiated APCs and fixed αCD3 for 7 d. ( C ). Th0 and Th17 cells were placed into routine CD8+ suppression assays as in prior figures (Th0 and Th17 controls). In parallel, Th17 cells, autologous APC, or CD8+ T cells were first incubated for 90 min with antibodies against IL-17RA, IL17-RC, or a combination of both. Cells were then washed and used in CD8+ suppression assays in a way that one of the cell types had been preincubated for receptor blockade. The bars indicate normalized suppression data (mean ± SEM), where the baseline suppression observed in the Th0 conditions was designated as 100%. * P
    Figure Legend Snippet: Reversal of Th17 suppressor resistance following neutralization of IL-17A, IL-17F, or IL-17AF cytokines or blockade of IL-17RA and/or IL-17RC on CD4+ T cells, but not on CD8+ T cells or APC. Naïve CD4+CD25- T cells obtained from healthy donor PBMCs were cultured in Th0 conditions ( A ) or under Th17 differentiation conditions ( B ). Differentiated Th subsets were CFSE-stained and incubated with various IL-17 cytokine neutralizing antibodies, as indicated, and then placed in suppression assays with autologous CD8+ T cells and irradiated APCs and fixed αCD3 for 7 d. ( C ). Th0 and Th17 cells were placed into routine CD8+ suppression assays as in prior figures (Th0 and Th17 controls). In parallel, Th17 cells, autologous APC, or CD8+ T cells were first incubated for 90 min with antibodies against IL-17RA, IL17-RC, or a combination of both. Cells were then washed and used in CD8+ suppression assays in a way that one of the cell types had been preincubated for receptor blockade. The bars indicate normalized suppression data (mean ± SEM), where the baseline suppression observed in the Th0 conditions was designated as 100%. * P

    Techniques Used: Neutralization, Cell Culture, Staining, Incubation, Irradiation

    Exposure of bulk (non-Th17) CD4+ T cells to exogenous IL-17A, IL-17F, or IL-17AF results in acquisition of resistance to immune suppression. Bulk ex vivo CD4+CD25- T cells were activated in the presence of indicated IL-17 cytokines (10 ng/mL each) for 7 d, followed by washing, CFSE staining, and suppression assays using autologous APC, CD8 T cells, and fixed αCD3. ( A ) represents %proliferation (mean ± SEM) of these cells in the absence of CD8+ T cells (1:0 condition). B – E represent mean %suppression ± SEM. * P
    Figure Legend Snippet: Exposure of bulk (non-Th17) CD4+ T cells to exogenous IL-17A, IL-17F, or IL-17AF results in acquisition of resistance to immune suppression. Bulk ex vivo CD4+CD25- T cells were activated in the presence of indicated IL-17 cytokines (10 ng/mL each) for 7 d, followed by washing, CFSE staining, and suppression assays using autologous APC, CD8 T cells, and fixed αCD3. ( A ) represents %proliferation (mean ± SEM) of these cells in the absence of CD8+ T cells (1:0 condition). B – E represent mean %suppression ± SEM. * P

    Techniques Used: Ex Vivo, Staining

    ( A ) IL-17 exposure induces IL-6– and IL-1β–related pathways, which, in turn, mediate effector CD4 T cell resistance to suppression. Canonical pathway enrichment using IPA for IL-17A–, IL-17F–, and IL-17AF–treated CD4+CD25- cells, compared to media alone, using RNA-seq data derived from each condition ( n = 3). Highlighted pathways had a P
    Figure Legend Snippet: ( A ) IL-17 exposure induces IL-6– and IL-1β–related pathways, which, in turn, mediate effector CD4 T cell resistance to suppression. Canonical pathway enrichment using IPA for IL-17A–, IL-17F–, and IL-17AF–treated CD4+CD25- cells, compared to media alone, using RNA-seq data derived from each condition ( n = 3). Highlighted pathways had a P

    Techniques Used: Indirect Immunoperoxidase Assay, RNA Sequencing Assay, Derivative Assay

    Related Articles

    Recombinant:

    Article Title: CD4 T cell-intrinsic role for the T helper 17 signature cytokine IL-17: Effector resistance to immune suppression
    Article Snippet: As indicated in some of the assays, the following neutralizing antibodies were added at 7 μg/mL: anti-IL-17A (eBioscience, 16-7178-85), anti-IL-17F (eBioscience, 16-7169-85), anti-IL-17AF (R & D Systems, AF317-NA), anti-IL-21 (LSBio, LS-C104584), anti-IL-22 (eBioscience, 16-7222-85). .. In some experiments, recombinant human cytokines IL17A (eBioscience, 34-8179-82), IL17F (R & D Systems, 1335-IL-025/CF)- and IL17AF (R & D Systems, 5194-IL-025/CF) were used at 10 ng/mL each. ..

    Article Title: Cytokines TNF-α, IL-6, IL-17F, and IL-4 Differentially Affect Osteogenic Differentiation of Human Adipose Stem Cells
    Article Snippet: After cytokine stimulation, the medium was replaced with osteogenic medium (OM), consisting of α -MEM containing 1% PSF, 10 IU/mL heparin, 2% human platelet lysate, 50 μ M ascorbic acid-2-phosphate (vitamin C; Sigma, St. Louis, MO, USA), 5 mM β -glycerophosphate (β GP; Sigma), and 10 nM 1,25-(OH)2 vitamin D3 (Sigma). .. Recombinant human TNF-α (R & D Systems, Minneapolis, MN, USA), recombinant human IL-4 (R & D Systems), recombinant human IL-6 (R & D Systems), recombinant human IL-6Rα (R & D Systems), recombinant human IL-8 (R & D Systems), and recombinant human IL-17F (R & D Systems) were added to the OM at 10 ng/mL and incubated for 72 h at 37°C in 5% CO2 in air. ..

    other:

    Article Title: Role of IL-17A, IL-17F, and the IL-17 Receptor in Regulating Growth-Related Oncogene-α and Granulocyte Colony-Stimulating Factor in Bronchial Epithelium: Implications for Airway Inflammation in Cystic Fibrosis 1
    Article Snippet: Human IL-17F was measured using Abs provided by Wyeth.

    Incubation:

    Article Title: Cytokines TNF-α, IL-6, IL-17F, and IL-4 Differentially Affect Osteogenic Differentiation of Human Adipose Stem Cells
    Article Snippet: After cytokine stimulation, the medium was replaced with osteogenic medium (OM), consisting of α -MEM containing 1% PSF, 10 IU/mL heparin, 2% human platelet lysate, 50 μ M ascorbic acid-2-phosphate (vitamin C; Sigma, St. Louis, MO, USA), 5 mM β -glycerophosphate (β GP; Sigma), and 10 nM 1,25-(OH)2 vitamin D3 (Sigma). .. Recombinant human TNF-α (R & D Systems, Minneapolis, MN, USA), recombinant human IL-4 (R & D Systems), recombinant human IL-6 (R & D Systems), recombinant human IL-6Rα (R & D Systems), recombinant human IL-8 (R & D Systems), and recombinant human IL-17F (R & D Systems) were added to the OM at 10 ng/mL and incubated for 72 h at 37°C in 5% CO2 in air. ..

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  • 93
    R&D Systems recombinant human il 17f protein cf
    Reversal of Th17 suppressor resistance following neutralization of IL-17A, <t>IL-17F,</t> or IL-17AF cytokines or blockade of IL-17RA and/or IL-17RC on CD4+ T cells, but not on CD8+ T cells or APC. Naïve CD4+CD25- T cells obtained from healthy donor PBMCs were cultured in Th0 conditions ( A ) or under Th17 differentiation conditions ( B ). Differentiated Th subsets were CFSE-stained and incubated with various IL-17 cytokine neutralizing antibodies, as indicated, and then placed in suppression assays with autologous CD8+ T cells and irradiated APCs and fixed αCD3 for 7 d. ( C ). Th0 and Th17 cells were placed into routine CD8+ suppression assays as in prior figures (Th0 and Th17 controls). In parallel, Th17 cells, autologous APC, or CD8+ T cells were first incubated for 90 min with antibodies against IL-17RA, IL17-RC, or a combination of both. Cells were then washed and used in CD8+ suppression assays in a way that one of the cell types had been preincubated for receptor blockade. The bars indicate normalized suppression data (mean ± SEM), where the baseline suppression observed in the Th0 conditions was designated as 100%. * P
    Recombinant Human Il 17f Protein Cf, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/recombinant human il 17f protein cf/product/R&D Systems
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    recombinant human il 17f protein cf - by Bioz Stars, 2021-07
    93/100 stars
      Buy from Supplier

    94
    R&D Systems il 17c
    Increased pro-inflammatory mediator production in <t>IL-17C−/−</t> colons. ( A ) Proximal, intermediate, and distal colon sections from DSS animals were pooled prior to mRNA isolation and gene quantification by real time PCR. n = 5 animals per
    Il 17c, supplied by R&D Systems, 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/il 17c/product/R&D Systems
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    il 17c - by Bioz Stars, 2021-07
    94/100 stars
      Buy from Supplier

    92
    R&D Systems recombinant human rh il 17a
    JNK1-dependent IL-17 and TGF-β signaling. The binding of <t>IL-17A/F</t> to the IL-17RA/IL-17RC receptor facilitates the recruitment of ACT1 to the receptor, which mediates the activation of JNK1, ERK, p38, and NF-κB (p65/p50) signaling, leading to the production of pro-inflammatory cytokines and chemokines (e.g. CXCL1 , IL6 ). Similarly, TGF-β binds to its receptor (TGFBR1/TGFBR2), leading to the activation of JNK1, ERK, p38, and SMAD (SMAD2/3/4) signaling. This pathway ultimately results in the production of extracellular matrix proteins and regulators (e.g. FN1 , IL11 ). The mutation (yellow star) in JNK1 impairs the JNK1-dependent activation of downstream AP-1 (c-Jun/ATF-2), thereby reducing the JNK1-dependent cellular responses to IL-17 and TGF-β.
    Recombinant Human Rh Il 17a, supplied by R&D Systems, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/recombinant human rh il 17a/product/R&D Systems
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    recombinant human rh il 17a - by Bioz Stars, 2021-07
    92/100 stars
      Buy from Supplier

    N/A
    The Recombinant Human IL 17F NS0 expressed Protein from R D Systems is derived from NS0 The Recombinant Human IL 17F NS0 expressed Protein has been validated for the following
      Buy from Supplier

    Image Search Results


    Reversal of Th17 suppressor resistance following neutralization of IL-17A, IL-17F, or IL-17AF cytokines or blockade of IL-17RA and/or IL-17RC on CD4+ T cells, but not on CD8+ T cells or APC. Naïve CD4+CD25- T cells obtained from healthy donor PBMCs were cultured in Th0 conditions ( A ) or under Th17 differentiation conditions ( B ). Differentiated Th subsets were CFSE-stained and incubated with various IL-17 cytokine neutralizing antibodies, as indicated, and then placed in suppression assays with autologous CD8+ T cells and irradiated APCs and fixed αCD3 for 7 d. ( C ). Th0 and Th17 cells were placed into routine CD8+ suppression assays as in prior figures (Th0 and Th17 controls). In parallel, Th17 cells, autologous APC, or CD8+ T cells were first incubated for 90 min with antibodies against IL-17RA, IL17-RC, or a combination of both. Cells were then washed and used in CD8+ suppression assays in a way that one of the cell types had been preincubated for receptor blockade. The bars indicate normalized suppression data (mean ± SEM), where the baseline suppression observed in the Th0 conditions was designated as 100%. * P

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

    Article Title: CD4 T cell-intrinsic role for the T helper 17 signature cytokine IL-17: Effector resistance to immune suppression

    doi: 10.1073/pnas.2005010117

    Figure Lengend Snippet: Reversal of Th17 suppressor resistance following neutralization of IL-17A, IL-17F, or IL-17AF cytokines or blockade of IL-17RA and/or IL-17RC on CD4+ T cells, but not on CD8+ T cells or APC. Naïve CD4+CD25- T cells obtained from healthy donor PBMCs were cultured in Th0 conditions ( A ) or under Th17 differentiation conditions ( B ). Differentiated Th subsets were CFSE-stained and incubated with various IL-17 cytokine neutralizing antibodies, as indicated, and then placed in suppression assays with autologous CD8+ T cells and irradiated APCs and fixed αCD3 for 7 d. ( C ). Th0 and Th17 cells were placed into routine CD8+ suppression assays as in prior figures (Th0 and Th17 controls). In parallel, Th17 cells, autologous APC, or CD8+ T cells were first incubated for 90 min with antibodies against IL-17RA, IL17-RC, or a combination of both. Cells were then washed and used in CD8+ suppression assays in a way that one of the cell types had been preincubated for receptor blockade. The bars indicate normalized suppression data (mean ± SEM), where the baseline suppression observed in the Th0 conditions was designated as 100%. * P

    Article Snippet: In some experiments, recombinant human cytokines IL17A (eBioscience, 34-8179-82), IL17F (R & D Systems, 1335-IL-025/CF)- and IL17AF (R & D Systems, 5194-IL-025/CF) were used at 10 ng/mL each.

    Techniques: Neutralization, Cell Culture, Staining, Incubation, Irradiation

    Exposure of bulk (non-Th17) CD4+ T cells to exogenous IL-17A, IL-17F, or IL-17AF results in acquisition of resistance to immune suppression. Bulk ex vivo CD4+CD25- T cells were activated in the presence of indicated IL-17 cytokines (10 ng/mL each) for 7 d, followed by washing, CFSE staining, and suppression assays using autologous APC, CD8 T cells, and fixed αCD3. ( A ) represents %proliferation (mean ± SEM) of these cells in the absence of CD8+ T cells (1:0 condition). B – E represent mean %suppression ± SEM. * P

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

    Article Title: CD4 T cell-intrinsic role for the T helper 17 signature cytokine IL-17: Effector resistance to immune suppression

    doi: 10.1073/pnas.2005010117

    Figure Lengend Snippet: Exposure of bulk (non-Th17) CD4+ T cells to exogenous IL-17A, IL-17F, or IL-17AF results in acquisition of resistance to immune suppression. Bulk ex vivo CD4+CD25- T cells were activated in the presence of indicated IL-17 cytokines (10 ng/mL each) for 7 d, followed by washing, CFSE staining, and suppression assays using autologous APC, CD8 T cells, and fixed αCD3. ( A ) represents %proliferation (mean ± SEM) of these cells in the absence of CD8+ T cells (1:0 condition). B – E represent mean %suppression ± SEM. * P

    Article Snippet: In some experiments, recombinant human cytokines IL17A (eBioscience, 34-8179-82), IL17F (R & D Systems, 1335-IL-025/CF)- and IL17AF (R & D Systems, 5194-IL-025/CF) were used at 10 ng/mL each.

    Techniques: Ex Vivo, Staining

    ( A ) IL-17 exposure induces IL-6– and IL-1β–related pathways, which, in turn, mediate effector CD4 T cell resistance to suppression. Canonical pathway enrichment using IPA for IL-17A–, IL-17F–, and IL-17AF–treated CD4+CD25- cells, compared to media alone, using RNA-seq data derived from each condition ( n = 3). Highlighted pathways had a P

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

    Article Title: CD4 T cell-intrinsic role for the T helper 17 signature cytokine IL-17: Effector resistance to immune suppression

    doi: 10.1073/pnas.2005010117

    Figure Lengend Snippet: ( A ) IL-17 exposure induces IL-6– and IL-1β–related pathways, which, in turn, mediate effector CD4 T cell resistance to suppression. Canonical pathway enrichment using IPA for IL-17A–, IL-17F–, and IL-17AF–treated CD4+CD25- cells, compared to media alone, using RNA-seq data derived from each condition ( n = 3). Highlighted pathways had a P

    Article Snippet: In some experiments, recombinant human cytokines IL17A (eBioscience, 34-8179-82), IL17F (R & D Systems, 1335-IL-025/CF)- and IL17AF (R & D Systems, 5194-IL-025/CF) were used at 10 ng/mL each.

    Techniques: Indirect Immunoperoxidase Assay, RNA Sequencing Assay, Derivative Assay

    Increased pro-inflammatory mediator production in IL-17C−/− colons. ( A ) Proximal, intermediate, and distal colon sections from DSS animals were pooled prior to mRNA isolation and gene quantification by real time PCR. n = 5 animals per

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

    Article Title: Regulation of intestinal inflammation and barrier function by IL-17C

    doi: 10.4049/jimmunol.1103014

    Figure Lengend Snippet: Increased pro-inflammatory mediator production in IL-17C−/− colons. ( A ) Proximal, intermediate, and distal colon sections from DSS animals were pooled prior to mRNA isolation and gene quantification by real time PCR. n = 5 animals per

    Article Snippet: To further characterize the intestinal T cell responses in IL-17C−/− animals, we directly isolated infiltrating leukocytes from the colons of diseased animals.

    Techniques: Isolation, Real-time Polymerase Chain Reaction

    IL-17C deficiency results in exacerbated DSS-induced colitis. ( A ) WT colon tissue samples were harvested from healthy animals (n = 4) or animals after 8 d DSS treatment (n = 16) and then analyzed for the expression of IL-17C mRNA by real time PCR. ( B

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

    Article Title: Regulation of intestinal inflammation and barrier function by IL-17C

    doi: 10.4049/jimmunol.1103014

    Figure Lengend Snippet: IL-17C deficiency results in exacerbated DSS-induced colitis. ( A ) WT colon tissue samples were harvested from healthy animals (n = 4) or animals after 8 d DSS treatment (n = 16) and then analyzed for the expression of IL-17C mRNA by real time PCR. ( B

    Article Snippet: To further characterize the intestinal T cell responses in IL-17C−/− animals, we directly isolated infiltrating leukocytes from the colons of diseased animals.

    Techniques: Expressing, Real-time Polymerase Chain Reaction

    IL-17C-IL-17RE signaling promotes tight junction protein expression. ( A ) YAMC cells were examined for IL-17RE expression by real-time RT-PCR. Bone marrow-derived dendritic cells (DC), naïve CD4+ T cells (nCD4), and Th17 cells were utilized as

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

    Article Title: Regulation of intestinal inflammation and barrier function by IL-17C

    doi: 10.4049/jimmunol.1103014

    Figure Lengend Snippet: IL-17C-IL-17RE signaling promotes tight junction protein expression. ( A ) YAMC cells were examined for IL-17RE expression by real-time RT-PCR. Bone marrow-derived dendritic cells (DC), naïve CD4+ T cells (nCD4), and Th17 cells were utilized as

    Article Snippet: To further characterize the intestinal T cell responses in IL-17C−/− animals, we directly isolated infiltrating leukocytes from the colons of diseased animals.

    Techniques: Expressing, Quantitative RT-PCR, Derivative Assay

    Characterization of the immune cell infiltrate in K5-IL-17C mouse skin

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

    Article Title: Keratinocyte overexpression of IL-17C promotes psoriasiform skin inflammation

    doi: 10.4049/jimmunol.1201505

    Figure Lengend Snippet: Characterization of the immune cell infiltrate in K5-IL-17C mouse skin

    Article Snippet: These results demonstrate similar mRNA transcript abundance of IL-17A and IL-17C but also illustrate that IL-17C protein is the most highly expressed IL-17 family member found in human involved psoriasis skin ( , 1058 ± 133 pg/mg IL-17C vs. 8 ± 2 pg/mg IL-17A protein).

    Techniques:

    Systemic inhibition of TNFα in K5-IL-17C mice leads to improvement in disease severity

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

    Article Title: Keratinocyte overexpression of IL-17C promotes psoriasiform skin inflammation

    doi: 10.4049/jimmunol.1201505

    Figure Lengend Snippet: Systemic inhibition of TNFα in K5-IL-17C mice leads to improvement in disease severity

    Article Snippet: These results demonstrate similar mRNA transcript abundance of IL-17A and IL-17C but also illustrate that IL-17C protein is the most highly expressed IL-17 family member found in human involved psoriasis skin ( , 1058 ± 133 pg/mg IL-17C vs. 8 ± 2 pg/mg IL-17A protein).

    Techniques: Inhibition, Mouse Assay

    IL-17C and TNFα induce characteristic psoriasis-related transcriptome genes in both additive and synergistic manners

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

    Article Title: Keratinocyte overexpression of IL-17C promotes psoriasiform skin inflammation

    doi: 10.4049/jimmunol.1201505

    Figure Lengend Snippet: IL-17C and TNFα induce characteristic psoriasis-related transcriptome genes in both additive and synergistic manners

    Article Snippet: These results demonstrate similar mRNA transcript abundance of IL-17A and IL-17C but also illustrate that IL-17C protein is the most highly expressed IL-17 family member found in human involved psoriasis skin ( , 1058 ± 133 pg/mg IL-17C vs. 8 ± 2 pg/mg IL-17A protein).

    Techniques:

    K5-IL-17C transgenic mice develop a psoriasiform skin phenotype

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

    Article Title: Keratinocyte overexpression of IL-17C promotes psoriasiform skin inflammation

    doi: 10.4049/jimmunol.1201505

    Figure Lengend Snippet: K5-IL-17C transgenic mice develop a psoriasiform skin phenotype

    Article Snippet: These results demonstrate similar mRNA transcript abundance of IL-17A and IL-17C but also illustrate that IL-17C protein is the most highly expressed IL-17 family member found in human involved psoriasis skin ( , 1058 ± 133 pg/mg IL-17C vs. 8 ± 2 pg/mg IL-17A protein).

    Techniques: Transgenic Assay, Mouse Assay

    K5-IL-17C mouse skin has increases in dermal angiogenesis and VEGF

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

    Article Title: Keratinocyte overexpression of IL-17C promotes psoriasiform skin inflammation

    doi: 10.4049/jimmunol.1201505

    Figure Lengend Snippet: K5-IL-17C mouse skin has increases in dermal angiogenesis and VEGF

    Article Snippet: These results demonstrate similar mRNA transcript abundance of IL-17A and IL-17C but also illustrate that IL-17C protein is the most highly expressed IL-17 family member found in human involved psoriasis skin ( , 1058 ± 133 pg/mg IL-17C vs. 8 ± 2 pg/mg IL-17A protein).

    Techniques:

    Psoriasis-related innate defense and cytokines/chemokines are increased in K5-IL-17C skin

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

    Article Title: Keratinocyte overexpression of IL-17C promotes psoriasiform skin inflammation

    doi: 10.4049/jimmunol.1201505

    Figure Lengend Snippet: Psoriasis-related innate defense and cytokines/chemokines are increased in K5-IL-17C skin

    Article Snippet: These results demonstrate similar mRNA transcript abundance of IL-17A and IL-17C but also illustrate that IL-17C protein is the most highly expressed IL-17 family member found in human involved psoriasis skin ( , 1058 ± 133 pg/mg IL-17C vs. 8 ± 2 pg/mg IL-17A protein).

    Techniques:

    IL-17C RNA and protein are increased in lesional psoriasis skin

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

    Article Title: Keratinocyte overexpression of IL-17C promotes psoriasiform skin inflammation

    doi: 10.4049/jimmunol.1201505

    Figure Lengend Snippet: IL-17C RNA and protein are increased in lesional psoriasis skin

    Article Snippet: These results demonstrate similar mRNA transcript abundance of IL-17A and IL-17C but also illustrate that IL-17C protein is the most highly expressed IL-17 family member found in human involved psoriasis skin ( , 1058 ± 133 pg/mg IL-17C vs. 8 ± 2 pg/mg IL-17A protein).

    Techniques:

    JNK1-dependent IL-17 and TGF-β signaling. The binding of IL-17A/F to the IL-17RA/IL-17RC receptor facilitates the recruitment of ACT1 to the receptor, which mediates the activation of JNK1, ERK, p38, and NF-κB (p65/p50) signaling, leading to the production of pro-inflammatory cytokines and chemokines (e.g. CXCL1 , IL6 ). Similarly, TGF-β binds to its receptor (TGFBR1/TGFBR2), leading to the activation of JNK1, ERK, p38, and SMAD (SMAD2/3/4) signaling. This pathway ultimately results in the production of extracellular matrix proteins and regulators (e.g. FN1 , IL11 ). The mutation (yellow star) in JNK1 impairs the JNK1-dependent activation of downstream AP-1 (c-Jun/ATF-2), thereby reducing the JNK1-dependent cellular responses to IL-17 and TGF-β.

    Journal: Science immunology

    Article Title: Chronic mucocutaneous candidiasis and connective tissue disorder in humans with impaired JNK1-dependent responses to IL-17A/F and TGF-β

    doi: 10.1126/sciimmunol.aax7965

    Figure Lengend Snippet: JNK1-dependent IL-17 and TGF-β signaling. The binding of IL-17A/F to the IL-17RA/IL-17RC receptor facilitates the recruitment of ACT1 to the receptor, which mediates the activation of JNK1, ERK, p38, and NF-κB (p65/p50) signaling, leading to the production of pro-inflammatory cytokines and chemokines (e.g. CXCL1 , IL6 ). Similarly, TGF-β binds to its receptor (TGFBR1/TGFBR2), leading to the activation of JNK1, ERK, p38, and SMAD (SMAD2/3/4) signaling. This pathway ultimately results in the production of extracellular matrix proteins and regulators (e.g. FN1 , IL11 ). The mutation (yellow star) in JNK1 impairs the JNK1-dependent activation of downstream AP-1 (c-Jun/ATF-2), thereby reducing the JNK1-dependent cellular responses to IL-17 and TGF-β.

    Article Snippet: After 24 h, cells were left unstimulated or were stimulated with recombinant human (rh) IL-17A (317-ILB; R & D Systems), rh IL-17F (1335-IL; R & D Systems), rh IL-17A/F (5194-IL; R & D Systems), rh TNF-α (210-TA; R & D Systems), rh IL-1β (201-LB; R & D Systems), rh lymphotoxin α1/β2 (8884-LY; R & D Systems), LTA-SA (tlrl-slta; InvivoGen), Pam3 CSK4 (tlrl-pms; InvivoGen), FSL-1 (tlrl-fsl; InvivoGen), Pam2 CSK4 (tlrl-pm2s-1; InvivoGen), and lipopolysaccharide (LPS) (L9764; Sigma-Aldrich) for a further 24 h. ELISA kits were used to determine the levels of GRO-α (DY275; R & D Systems), IL-6 (88-7066; Invitrogen), and IL-8 (M9318; Sanquin) in the supernatants.

    Techniques: Binding Assay, Activation Assay, Mutagenesis

    The MAPK8 variant impairs fibroblast responses to IL-17A/F. ( A ) Production of GRO-α (top panel) and IL-6 (bottom panel) by SV40-fibroblasts from healthy controls (C1 and C2), patients (P2 and P3), and an IL-17RA-deficient ( IL17RA −/− ) stimulated with IL-17A, IL-17F, or IL-17A/F (10, 100, or 1000 ng/mL) for 24 h. ( B ) Production of GRO-α (top panel) and IL-6 (bottom panel) by SV40-fibroblasts from healthy controls (C1 and C2), patients (P2 and P3), and a NEMO-deficient ( NEMO −/− ) stimulated with TNF-α (20 ng/mL) or IL-1β (10 ng/mL) for 24 h. ( C ) Production of GRO-α (top panel) and IL-6 (bottom panel) by SV40-fibroblasts from healthy controls (C1 and C2) and patients (P2 and P3) transfected with empty vector (EV) or plasmids encoding WT JNK1α1 (α1), JNK1α2 (α2), JNK1β1 (β1), JNK1β2 (β2), all four isoforms (α1/α2/β1/β2), JNK1ES (ES), or JNK1IR (IR), in the presence of IL-17A (100 ng/mL), for 24 h. ( D ) Production of GRO-α (left panel) and IL-6 (right panel) by primary fibroblasts from healthy controls (C1, C2, and C3) transfected with control siRNA (50 nM) or MAPK8 siRNA (50 nM) for 24 h and then stimulated with IL-17A (100 ng/mL) for an additional 24 h. The values shown are the means ± SEM of three independent experiments ( A-D ). *, P

    Journal: Science immunology

    Article Title: Chronic mucocutaneous candidiasis and connective tissue disorder in humans with impaired JNK1-dependent responses to IL-17A/F and TGF-β

    doi: 10.1126/sciimmunol.aax7965

    Figure Lengend Snippet: The MAPK8 variant impairs fibroblast responses to IL-17A/F. ( A ) Production of GRO-α (top panel) and IL-6 (bottom panel) by SV40-fibroblasts from healthy controls (C1 and C2), patients (P2 and P3), and an IL-17RA-deficient ( IL17RA −/− ) stimulated with IL-17A, IL-17F, or IL-17A/F (10, 100, or 1000 ng/mL) for 24 h. ( B ) Production of GRO-α (top panel) and IL-6 (bottom panel) by SV40-fibroblasts from healthy controls (C1 and C2), patients (P2 and P3), and a NEMO-deficient ( NEMO −/− ) stimulated with TNF-α (20 ng/mL) or IL-1β (10 ng/mL) for 24 h. ( C ) Production of GRO-α (top panel) and IL-6 (bottom panel) by SV40-fibroblasts from healthy controls (C1 and C2) and patients (P2 and P3) transfected with empty vector (EV) or plasmids encoding WT JNK1α1 (α1), JNK1α2 (α2), JNK1β1 (β1), JNK1β2 (β2), all four isoforms (α1/α2/β1/β2), JNK1ES (ES), or JNK1IR (IR), in the presence of IL-17A (100 ng/mL), for 24 h. ( D ) Production of GRO-α (left panel) and IL-6 (right panel) by primary fibroblasts from healthy controls (C1, C2, and C3) transfected with control siRNA (50 nM) or MAPK8 siRNA (50 nM) for 24 h and then stimulated with IL-17A (100 ng/mL) for an additional 24 h. The values shown are the means ± SEM of three independent experiments ( A-D ). *, P

    Article Snippet: After 24 h, cells were left unstimulated or were stimulated with recombinant human (rh) IL-17A (317-ILB; R & D Systems), rh IL-17F (1335-IL; R & D Systems), rh IL-17A/F (5194-IL; R & D Systems), rh TNF-α (210-TA; R & D Systems), rh IL-1β (201-LB; R & D Systems), rh lymphotoxin α1/β2 (8884-LY; R & D Systems), LTA-SA (tlrl-slta; InvivoGen), Pam3 CSK4 (tlrl-pms; InvivoGen), FSL-1 (tlrl-fsl; InvivoGen), Pam2 CSK4 (tlrl-pm2s-1; InvivoGen), and lipopolysaccharide (LPS) (L9764; Sigma-Aldrich) for a further 24 h. ELISA kits were used to determine the levels of GRO-α (DY275; R & D Systems), IL-6 (88-7066; Invitrogen), and IL-8 (M9318; Sanquin) in the supernatants.

    Techniques: Variant Assay, Transfection, Plasmid Preparation

    Compromised T-cell differentiation in the patients. ( A ) Percentage of total, naïve (CCR7 + CD45RA + ), central memory (CM; CCR7 + CD45RA − ), effector memory (EM; CCR7 − CD45RA − ), or CD45RA + effector memory (EMRA; CCR7 − CD45RA + ) CD4 + and CD8 + T cells from healthy controls ( n =40) and patients (P2 and P3). ( B ) Frequency of T H 1 (CXCR5 − CXCR3 + CCR6 − ), T H 2 (CXCR5 − CXCR3 − CCR6 − CCR4 + ), T H 17 (CXCR5 − CXCR3 − CCR6 + CCR4 + ), T H 1* (CXCR5 − CXCR3 + CCR6 + CCR4 + ), T FH (CXCR5 + ), and T reg (CD25 + FOXP3 + ) subsets among CD4 + T cells from healthy controls (T H 1, T H 2, T H 17, T H 1*, and T FH , n =34; T reg , n =17) and patients (P2 and P3). ( C ) Production of IL-17A and IL-22 by whole blood from healthy controls ( n =33) and patients (P2 and P3) after stimulation with PMA plus ionomycin for 24 h. ( D ) Percentage of IL-17A + , IL-17F + , and IFN-γ + cells among memory CD4 + T cells from healthy controls ( n =36) and patients (P2 and P3) activated by T-cell activation and expansion (TAE) beads or PMA plus ionomycin (P/I) for 12 h. ( E ) Cytokine production by naïve CD4 + T cells from healthy controls ( n =8) and patients (P2 and P3) cultured under T H 0-, T H 17- or T H 1-polarizing conditions. ( F and G ) Frequency of IL-17A + and IFN-γ + cells among naïve ( F ) and memory ( G ) CD4 + T cells from healthy controls ( n =10) and patients (P2 and P3) cultured under T H 0-, T H 17- or T H 1-polarizing conditions. C, Healthy controls; P, P2 and P3. Horizontal bars represent median values ( A-G) . *, P

    Journal: Science immunology

    Article Title: Chronic mucocutaneous candidiasis and connective tissue disorder in humans with impaired JNK1-dependent responses to IL-17A/F and TGF-β

    doi: 10.1126/sciimmunol.aax7965

    Figure Lengend Snippet: Compromised T-cell differentiation in the patients. ( A ) Percentage of total, naïve (CCR7 + CD45RA + ), central memory (CM; CCR7 + CD45RA − ), effector memory (EM; CCR7 − CD45RA − ), or CD45RA + effector memory (EMRA; CCR7 − CD45RA + ) CD4 + and CD8 + T cells from healthy controls ( n =40) and patients (P2 and P3). ( B ) Frequency of T H 1 (CXCR5 − CXCR3 + CCR6 − ), T H 2 (CXCR5 − CXCR3 − CCR6 − CCR4 + ), T H 17 (CXCR5 − CXCR3 − CCR6 + CCR4 + ), T H 1* (CXCR5 − CXCR3 + CCR6 + CCR4 + ), T FH (CXCR5 + ), and T reg (CD25 + FOXP3 + ) subsets among CD4 + T cells from healthy controls (T H 1, T H 2, T H 17, T H 1*, and T FH , n =34; T reg , n =17) and patients (P2 and P3). ( C ) Production of IL-17A and IL-22 by whole blood from healthy controls ( n =33) and patients (P2 and P3) after stimulation with PMA plus ionomycin for 24 h. ( D ) Percentage of IL-17A + , IL-17F + , and IFN-γ + cells among memory CD4 + T cells from healthy controls ( n =36) and patients (P2 and P3) activated by T-cell activation and expansion (TAE) beads or PMA plus ionomycin (P/I) for 12 h. ( E ) Cytokine production by naïve CD4 + T cells from healthy controls ( n =8) and patients (P2 and P3) cultured under T H 0-, T H 17- or T H 1-polarizing conditions. ( F and G ) Frequency of IL-17A + and IFN-γ + cells among naïve ( F ) and memory ( G ) CD4 + T cells from healthy controls ( n =10) and patients (P2 and P3) cultured under T H 0-, T H 17- or T H 1-polarizing conditions. C, Healthy controls; P, P2 and P3. Horizontal bars represent median values ( A-G) . *, P

    Article Snippet: After 24 h, cells were left unstimulated or were stimulated with recombinant human (rh) IL-17A (317-ILB; R & D Systems), rh IL-17F (1335-IL; R & D Systems), rh IL-17A/F (5194-IL; R & D Systems), rh TNF-α (210-TA; R & D Systems), rh IL-1β (201-LB; R & D Systems), rh lymphotoxin α1/β2 (8884-LY; R & D Systems), LTA-SA (tlrl-slta; InvivoGen), Pam3 CSK4 (tlrl-pms; InvivoGen), FSL-1 (tlrl-fsl; InvivoGen), Pam2 CSK4 (tlrl-pm2s-1; InvivoGen), and lipopolysaccharide (LPS) (L9764; Sigma-Aldrich) for a further 24 h. ELISA kits were used to determine the levels of GRO-α (DY275; R & D Systems), IL-6 (88-7066; Invitrogen), and IL-8 (M9318; Sanquin) in the supernatants.

    Techniques: Cell Differentiation, Activation Assay, Cell Culture