il 17f  (R&D Systems)

 
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    Name:
    Human Primate IL 17F Antibody
    Description:
    The Human Primate IL 17F Antibody from R D Systems is a goat polyclonal antibody to IL 17F This antibody reacts with human primate The Human Primate IL 17F Antibody has been validated for the following applications Western Blot Immunocytochemistry ELISA Capture Matched Antibody Pair
    Catalog Number:
    AF1335
    Price:
    375
    Category:
    Primary Antibodies
    Applications:
    Western Blot, Immunocytochemistry, ELISA Capture (Matched Antibody Pair)
    Purity:
    Antigen Affinity-purified
    Conjugate:
    Unconjugated
    Immunogen:
    E. coli-derived recombinant human IL-17F (R&D Systems, Catalog # 1335-IL), Arg31-Gln163, Accession # AAK83350
    Size:
    100 ug
    Host:
    Goat
    Isotype:
    IgG
    Buy from Supplier


    Structured Review

    R&D Systems il 17f
    Immunostaining for chemoattractant receptor CXCR1/IL-8RA and <t>IL-17F</t> in representative samples of prostates from C57BL/6J mice. IL-1 β (10 μg/kg) was i.v. injected in the tail vein. To proof pro-inflammatory ability of IL-1 β along
    The Human Primate IL 17F Antibody from R D Systems is a goat polyclonal antibody to IL 17F This antibody reacts with human primate The Human Primate IL 17F Antibody has been validated for the following applications Western Blot Immunocytochemistry ELISA Capture Matched Antibody Pair
    https://www.bioz.com/result/il 17f/product/R&D Systems
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    il 17f - by Bioz Stars, 2021-06
    92/100 stars

    Images

    1) Product Images from "IL-1?-INDUCED POST-TRANSITION EFFECT OF NF-KAPPAB PROVIDES TIME-DEPENDENT WAVE OF SIGNALS FOR INITIAL PHASE OF INTRAPOSTATIC INFLAMMATION"

    Article Title: IL-1?-INDUCED POST-TRANSITION EFFECT OF NF-KAPPAB PROVIDES TIME-DEPENDENT WAVE OF SIGNALS FOR INITIAL PHASE OF INTRAPOSTATIC INFLAMMATION

    Journal:

    doi: 10.1002/pros.20916

    Immunostaining for chemoattractant receptor CXCR1/IL-8RA and IL-17F in representative samples of prostates from C57BL/6J mice. IL-1 β (10 μg/kg) was i.v. injected in the tail vein. To proof pro-inflammatory ability of IL-1 β along
    Figure Legend Snippet: Immunostaining for chemoattractant receptor CXCR1/IL-8RA and IL-17F in representative samples of prostates from C57BL/6J mice. IL-1 β (10 μg/kg) was i.v. injected in the tail vein. To proof pro-inflammatory ability of IL-1 β along

    Techniques Used: Immunostaining, Mouse Assay, Injection

    Systemic administration of IL-1β induces multitype time-dependent behavior of intraprostatic chemoattractant receptors and IL-17F
    Figure Legend Snippet: Systemic administration of IL-1β induces multitype time-dependent behavior of intraprostatic chemoattractant receptors and IL-17F

    Techniques Used:

    2) Product Images from "Aggravated Atherosclerosis and Vascular Inflammation With Reduced Kidney Function Depend on Interleukin-17 Receptor A and Are Normalized by Inhibition of Interleukin-17A"

    Article Title: Aggravated Atherosclerosis and Vascular Inflammation With Reduced Kidney Function Depend on Interleukin-17 Receptor A and Are Normalized by Inhibition of Interleukin-17A

    Journal: JACC: Basic to Translational Science

    doi: 10.1016/j.jacbts.2017.08.005

    IL-17A Promotes Inflammatory Cytokine Expression in Endothelial Cells (A) IL-17 receptor A ( Il17ra ) and auxiliary subunits Il17rc and Il17re mRNA expression was determined by using quantitative polymerase chain reaction (qPCR). Il17rb messenger ribonucleic acid (mRNA) was below detection limit (n = 4, 2 exp.). (B to I) Endothelial cells were stimulated for 2 h with 50 ng/ml IL-17A (B to E) or IL-17F (F to I) . CCL2 (B and F) , CXCL1 (C and G) , IL-6 (D and H) , and granulocyte-macrophage colony-stimulating factor (GM-CSF) (E and I) cytokine expression quantified by using qPCR (n = 8 from 4 independent experiments for each cytokine).
    Figure Legend Snippet: IL-17A Promotes Inflammatory Cytokine Expression in Endothelial Cells (A) IL-17 receptor A ( Il17ra ) and auxiliary subunits Il17rc and Il17re mRNA expression was determined by using quantitative polymerase chain reaction (qPCR). Il17rb messenger ribonucleic acid (mRNA) was below detection limit (n = 4, 2 exp.). (B to I) Endothelial cells were stimulated for 2 h with 50 ng/ml IL-17A (B to E) or IL-17F (F to I) . CCL2 (B and F) , CXCL1 (C and G) , IL-6 (D and H) , and granulocyte-macrophage colony-stimulating factor (GM-CSF) (E and I) cytokine expression quantified by using qPCR (n = 8 from 4 independent experiments for each cytokine).

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction

    3) Product Images from "Leptin facilitates the differentiation of Th17 cells from MRL/Mp-Fas lpr lupus mice by activating NLRP3 inflammasome"

    Article Title: Leptin facilitates the differentiation of Th17 cells from MRL/Mp-Fas lpr lupus mice by activating NLRP3 inflammasome

    Journal: Innate Immunity

    doi: 10.1177/1753425919886643

    Leptin promotes the differentiation of Th17 cells from MRL/lpr lupus mice. mRNA levels of (a) IL-17A, (b) IL-17F, and (c) RORγt by qPCR and (d) IL-17A and (e) IL-17F by ELISA in CD4 + T cells from MRL/lpr lupus mice stimulated under Th17 polarizing conditions and treated with leptin at scalar doses during the last 18 h of culture. Flow cytometry results of CD4 + IL-17 + from CD4 + T cells treated as above. (g) Representative and (F) cumulative data from two experiments ( n = 10). *P
    Figure Legend Snippet: Leptin promotes the differentiation of Th17 cells from MRL/lpr lupus mice. mRNA levels of (a) IL-17A, (b) IL-17F, and (c) RORγt by qPCR and (d) IL-17A and (e) IL-17F by ELISA in CD4 + T cells from MRL/lpr lupus mice stimulated under Th17 polarizing conditions and treated with leptin at scalar doses during the last 18 h of culture. Flow cytometry results of CD4 + IL-17 + from CD4 + T cells treated as above. (g) Representative and (F) cumulative data from two experiments ( n = 10). *P

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

    4) Product Images from "Elucidating the role of interleukin-17F in cutaneous T-cell lymphoma"

    Article Title: Elucidating the role of interleukin-17F in cutaneous T-cell lymphoma

    Journal: Blood

    doi: 10.1182/blood-2013-01-480889

    High lesional expression of IL-17F is associated with progressive disease. Kaplan-Meier analyses of (A) disease progression and (B) disease-specific survival in the Boston historic cohort of CTCL patients (n = 60) stratified according to IL-17F mRNA expression
    Figure Legend Snippet: High lesional expression of IL-17F is associated with progressive disease. Kaplan-Meier analyses of (A) disease progression and (B) disease-specific survival in the Boston historic cohort of CTCL patients (n = 60) stratified according to IL-17F mRNA expression

    Techniques Used: Expressing

    IL-17F expression correlates with increased risk of disease progression
    Figure Legend Snippet: IL-17F expression correlates with increased risk of disease progression

    Techniques Used: Expressing

    The Jak/Stat3 pathway promotes the expression of IL-17F in malignant T cells. (A) Malignant T cells (PB2B) were incubated with Jak inhibitors (Jak3 inhibitor II/WHI-P154, 40 µM; Jak inhibitor I/P6, 1 µM), an inhibitor against Stat3 (Sta-21,
    Figure Legend Snippet: The Jak/Stat3 pathway promotes the expression of IL-17F in malignant T cells. (A) Malignant T cells (PB2B) were incubated with Jak inhibitors (Jak3 inhibitor II/WHI-P154, 40 µM; Jak inhibitor I/P6, 1 µM), an inhibitor against Stat3 (Sta-21,

    Techniques Used: Expressing, Incubation

    Quantification of IL-17F and IL-17A mRNA in MF and benign skin biopsies. Skin biopsies were obtained from individuals with MF, chronic dermatitis (CD), psoriasis (PSO), and volunteers with normal healthy skin (NS) and used for RNA extraction as described
    Figure Legend Snippet: Quantification of IL-17F and IL-17A mRNA in MF and benign skin biopsies. Skin biopsies were obtained from individuals with MF, chronic dermatitis (CD), psoriasis (PSO), and volunteers with normal healthy skin (NS) and used for RNA extraction as described

    Techniques Used: RNA Extraction

    Quantification of IL-17F and IL-17A mRNA in CD4 T cells isolated from the blood of SS patients and healthy donors. RNA purified from CD4 T cells freshly isolated from the blood of healthy donors (HD) and patients with SS was subjected to QPCR using primers
    Figure Legend Snippet: Quantification of IL-17F and IL-17A mRNA in CD4 T cells isolated from the blood of SS patients and healthy donors. RNA purified from CD4 T cells freshly isolated from the blood of healthy donors (HD) and patients with SS was subjected to QPCR using primers

    Techniques Used: Isolation, Purification, Real-time Polymerase Chain Reaction

    Malignant CTCL cell lines express IL-17F and/or IL-17A. Nonmalignant (MySi) and malignant (MF2000, PB2B, SeZ-4, and SeAx) T-cell lines established from patients with CTCL were cultured for 24 hours in the absence (−) or presence (P + I) of PMA
    Figure Legend Snippet: Malignant CTCL cell lines express IL-17F and/or IL-17A. Nonmalignant (MySi) and malignant (MF2000, PB2B, SeZ-4, and SeAx) T-cell lines established from patients with CTCL were cultured for 24 hours in the absence (−) or presence (P + I) of PMA

    Techniques Used: Cell Culture

    5) Product Images from "Antibody blockade of IL-17 family cytokines in immunity to acute murine oral mucosal candidiasis"

    Article Title: Antibody blockade of IL-17 family cytokines in immunity to acute murine oral mucosal candidiasis

    Journal: Journal of Leukocyte Biology

    doi: 10.1189/jlb.4A0915-428R

    Anti-IL-17A antibodies but not anti-IL-17F antibodies render mice susceptible to OPC.
    Figure Legend Snippet: Anti-IL-17A antibodies but not anti-IL-17F antibodies render mice susceptible to OPC.

    Techniques Used: Mouse Assay

    6) Product Images from "Antibody blockade of IL-17 family cytokines in immunity to acute murine oral mucosal candidiasis"

    Article Title: Antibody blockade of IL-17 family cytokines in immunity to acute murine oral mucosal candidiasis

    Journal: Journal of Leukocyte Biology

    doi: 10.1189/jlb.4A0915-428R

    Anti-IL-17A antibodies but not anti-IL-17F antibodies render mice susceptible to OPC.
    Figure Legend Snippet: Anti-IL-17A antibodies but not anti-IL-17F antibodies render mice susceptible to OPC.

    Techniques Used: Mouse Assay

    7) Product Images from "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 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

    Journal:

    doi:

    Effects of blocking IL-17R on GRO- α ( A ) and G-CSF ( B ) production by IL-17A and IL-17F. Primary HBE cells were pretreated with IL-17R Ab (2 μ g/ml) 30 min before IL-17A and IL-17F treatment (both at 10 ng/ml). Apical and basolateral medium
    Figure Legend Snippet: Effects of blocking IL-17R on GRO- α ( A ) and G-CSF ( B ) production by IL-17A and IL-17F. Primary HBE cells were pretreated with IL-17R Ab (2 μ g/ml) 30 min before IL-17A and IL-17F treatment (both at 10 ng/ml). Apical and basolateral medium

    Techniques Used: Blocking Assay

    GRO- α ( A ) and G-CSF ( B ) secreted after stimulation with IL-17F and/or TNF- α . primary HBE cells were treated with IL-17F (10 ng/ml) and TNF- α (1 ng/ml). The cytokine mixture (IL-17F + TNF- α ) was also preincubated with anti-IL-17
    Figure Legend Snippet: GRO- α ( A ) and G-CSF ( B ) secreted after stimulation with IL-17F and/or TNF- α . primary HBE cells were treated with IL-17F (10 ng/ml) and TNF- α (1 ng/ml). The cytokine mixture (IL-17F + TNF- α ) was also preincubated with anti-IL-17

    Techniques Used:

    Cytokines levels in sputum from CF patients undergoing pulmonary exacerbation. Panel A: IL-17A and IL-17F concentration in sputum from CF patients at different time points, as indicated, were measured by ELISA. Panel B: IL-17- induced cytokines IL-8 (upper
    Figure Legend Snippet: Cytokines levels in sputum from CF patients undergoing pulmonary exacerbation. Panel A: IL-17A and IL-17F concentration in sputum from CF patients at different time points, as indicated, were measured by ELISA. Panel B: IL-17- induced cytokines IL-8 (upper

    Techniques Used: Concentration Assay, Enzyme-linked Immunosorbent Assay

    A , Dose-dependent elevation of GRO- α , G-CSF, and MCP-1 protein levels by recombinant human IL-17A and IL-17F. Primary HBE cells were treated with different doses of IL-17A and IL-17F, as indicated. Basolateral media were collected 24 h after the
    Figure Legend Snippet: A , Dose-dependent elevation of GRO- α , G-CSF, and MCP-1 protein levels by recombinant human IL-17A and IL-17F. Primary HBE cells were treated with different doses of IL-17A and IL-17F, as indicated. Basolateral media were collected 24 h after the

    Techniques Used: Recombinant

    IL-17A and IL-17F up-regulate G-CSF, GRO-α, and MCP-1 in HBE cells: kinetic studies
    Figure Legend Snippet: IL-17A and IL-17F up-regulate G-CSF, GRO-α, and MCP-1 in HBE cells: kinetic studies

    Techniques Used:

    8) Product Images from "Antibody blockade of IL-17 family cytokines in immunity to acute murine oral mucosal candidiasis"

    Article Title: Antibody blockade of IL-17 family cytokines in immunity to acute murine oral mucosal candidiasis

    Journal: Journal of Leukocyte Biology

    doi: 10.1189/jlb.4A0915-428R

    Anti-IL-17A antibodies but not anti-IL-17F antibodies render mice susceptible to OPC.
    Figure Legend Snippet: Anti-IL-17A antibodies but not anti-IL-17F antibodies render mice susceptible to OPC.

    Techniques Used: Mouse Assay

    9) Product Images from "IL-17F Induces CCL20 in Bronchial Epithelial Cells"

    Article Title: IL-17F Induces CCL20 in Bronchial Epithelial Cells

    Journal: Journal of Allergy

    doi: 10.1155/2011/587204

    Effect of overexpression of dominant-negative mutants Raf1 and Ras on CCL20 protein expression in BEAS-2B cells. The cells overexpressing dominant-negative mutants were stimulated with IL-17F for 24 hrs, and CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P
    Figure Legend Snippet: Effect of overexpression of dominant-negative mutants Raf1 and Ras on CCL20 protein expression in BEAS-2B cells. The cells overexpressing dominant-negative mutants were stimulated with IL-17F for 24 hrs, and CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P

    Techniques Used: Over Expression, Dominant Negative Mutation, Expressing, Enzyme-linked Immunosorbent Assay

    Effect of MSK1 inhibitors, H89, and Ro318220 on IL-17F-induced CCL20. BEAS-2B cells were pretreated for 1 hr as indicated before the 24-hr stimulation of IL-17F, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P
    Figure Legend Snippet: Effect of MSK1 inhibitors, H89, and Ro318220 on IL-17F-induced CCL20. BEAS-2B cells were pretreated for 1 hr as indicated before the 24-hr stimulation of IL-17F, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P

    Techniques Used: Enzyme-linked Immunosorbent Assay

    Effect of siRNA for p90RSK, MSK1 and CREB on IL-17F-induced CCL20 expression. BEAS-2B cells transfected with siRNAs as indicated were stimulated with IL-17F for 24 hrs, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as mean s ± SEM ( n = 6). * P
    Figure Legend Snippet: Effect of siRNA for p90RSK, MSK1 and CREB on IL-17F-induced CCL20 expression. BEAS-2B cells transfected with siRNAs as indicated were stimulated with IL-17F for 24 hrs, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as mean s ± SEM ( n = 6). * P

    Techniques Used: Expressing, Transfection, Enzyme-linked Immunosorbent Assay

    The expression of CCL20 gene and protein by IL-17F in bronchial epithelial cells. (a) CCL20 gene expression by real-time PCR in BEAS-2B cells. Real-time PCR was performed as described in Materials and Methods. BEAS-2B cells were stimulated with IL-17F for 4 hrs ( n = 6). (c) CCL20 protein levels in supernatants in BEAS-2B cells. ELISA was performed ( n = 6). (d) CCL20 protein levels in supernatants in NHBEs ( n = 6). * P
    Figure Legend Snippet: The expression of CCL20 gene and protein by IL-17F in bronchial epithelial cells. (a) CCL20 gene expression by real-time PCR in BEAS-2B cells. Real-time PCR was performed as described in Materials and Methods. BEAS-2B cells were stimulated with IL-17F for 4 hrs ( n = 6). (c) CCL20 protein levels in supernatants in BEAS-2B cells. ELISA was performed ( n = 6). (d) CCL20 protein levels in supernatants in NHBEs ( n = 6). * P

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

    Effect of PD98059 (PD), U0126, Raf1 kinase inhibitor I (Raf I), SB202190 (SB), and SP600125 (SP) on CCL20 protein expression in BEAS-2Bs. The cells were pretreated for 1 hr as indicated before the 24-hr stimulation of IL-17F, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P
    Figure Legend Snippet: Effect of PD98059 (PD), U0126, Raf1 kinase inhibitor I (Raf I), SB202190 (SB), and SP600125 (SP) on CCL20 protein expression in BEAS-2Bs. The cells were pretreated for 1 hr as indicated before the 24-hr stimulation of IL-17F, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P

    Techniques Used: Expressing, Enzyme-linked Immunosorbent Assay

    10) Product Images from "Expression of the T Helper 17-Associated Cytokines IL-17A and IL-17F in Asthma and COPD"

    Article Title: Expression of the T Helper 17-Associated Cytokines IL-17A and IL-17F in Asthma and COPD

    Journal: Chest

    doi: 10.1378/chest.09-3058

    IL-17A and IL-17F expression in the submucosa in COPD. Representative photomicrographs of proximal airway resections from COPD tissue, illustrating isotype control. A, Goat IgG. B, IL-17A + cells present in the submucosa. C, IL-17F + cells in the submucosa (× 400). IL-17A/F + cells highlighted by arrows. D, The number of IL-17A + and E, IL-17F + cells in the submucosa of healthy control subjects (never smokers), healthy control subjects (smokers), and subjects with COPD. P values for across-group comparison by Kruskal-Wallis test and Dunn post hoc test for between-group comparisons are as shown.
    Figure Legend Snippet: IL-17A and IL-17F expression in the submucosa in COPD. Representative photomicrographs of proximal airway resections from COPD tissue, illustrating isotype control. A, Goat IgG. B, IL-17A + cells present in the submucosa. C, IL-17F + cells in the submucosa (× 400). IL-17A/F + cells highlighted by arrows. D, The number of IL-17A + and E, IL-17F + cells in the submucosa of healthy control subjects (never smokers), healthy control subjects (smokers), and subjects with COPD. P values for across-group comparison by Kruskal-Wallis test and Dunn post hoc test for between-group comparisons are as shown.

    Techniques Used: Expressing

    IL-17A and IL-17F expression in the submucosa in asthma. Representative photomicrographs of bronchial biopsy sections from subjects with severe asthma, illustrating isotype control. A, Goat IgG. B, IL-17A + cells present in the bronchial submucosa. C, IL-17F + cells in the submucosa (× 400). IL-17A/F + cells highlighted by arrows. D, The number of IL-17A + and E, IL-17F + cells in the bronchial submucosa of healthy control subjects, subjects with mild to moderate asthma (Global Initiative for Asthma [GINA] 1-3), and subjects with severe asthma (GINA 4-5). P values for across-group comparison by Kruskal-Wallis test and Dunn post hoc test for between-group comparisons are as shown.
    Figure Legend Snippet: IL-17A and IL-17F expression in the submucosa in asthma. Representative photomicrographs of bronchial biopsy sections from subjects with severe asthma, illustrating isotype control. A, Goat IgG. B, IL-17A + cells present in the bronchial submucosa. C, IL-17F + cells in the submucosa (× 400). IL-17A/F + cells highlighted by arrows. D, The number of IL-17A + and E, IL-17F + cells in the bronchial submucosa of healthy control subjects, subjects with mild to moderate asthma (Global Initiative for Asthma [GINA] 1-3), and subjects with severe asthma (GINA 4-5). P values for across-group comparison by Kruskal-Wallis test and Dunn post hoc test for between-group comparisons are as shown.

    Techniques Used: Expressing

    11) Product Images from "Interleukin-17A is involved in mechanical hyperalgesia but not in the severity of murine antigen-induced arthritis"

    Article Title: Interleukin-17A is involved in mechanical hyperalgesia but not in the severity of murine antigen-induced arthritis

    Journal: Scientific Reports

    doi: 10.1038/s41598-017-10509-5

    Effects of IL-17 family members on TTX-resistant and TTX-sensitive Na + currents in isolated and cultured DRG neurones and CGRP release in vitro from DRG neurones from naïve WT mice. ( a – d ) Changes of I max (peak current densities) in DRG neurones after bath application of IL-17B (n = 5) ( a ), IL-17C (n = 5) ( b ), IL-17D (n = 7) ( c ), and IL-17F (n = 7) ( d ). Only the neurones were included which showed increases of TTX-R currents, as indicated in ( e ). ( e ) I max of TTX-R currents of all neurones tested with IL-17 family members. No compound was applied to control neurones. ( f ) Changes of TTX-S Na + currents (I max ) in DRG neurones after bath application of IL-17 family members. No compound was applied to control neurones. ( g ) Release of CGRP from DRG neurones in vitro after cell culture for 48 h and depolarization with KCl and stimulation with IL-17A for 20 min (n = 5 per group). Illustrated CGRP concentrations show the evoked release minus the basal production in the same time in relation to total protein concentration of the DRG cell cultures. Although no significant differences in the release of CGRP between WT and IL-17KO were detectable, IL-17A (10 ng/ml) signalling increases CGRP release in WT DRG neurones (p = 0.045). *p
    Figure Legend Snippet: Effects of IL-17 family members on TTX-resistant and TTX-sensitive Na + currents in isolated and cultured DRG neurones and CGRP release in vitro from DRG neurones from naïve WT mice. ( a – d ) Changes of I max (peak current densities) in DRG neurones after bath application of IL-17B (n = 5) ( a ), IL-17C (n = 5) ( b ), IL-17D (n = 7) ( c ), and IL-17F (n = 7) ( d ). Only the neurones were included which showed increases of TTX-R currents, as indicated in ( e ). ( e ) I max of TTX-R currents of all neurones tested with IL-17 family members. No compound was applied to control neurones. ( f ) Changes of TTX-S Na + currents (I max ) in DRG neurones after bath application of IL-17 family members. No compound was applied to control neurones. ( g ) Release of CGRP from DRG neurones in vitro after cell culture for 48 h and depolarization with KCl and stimulation with IL-17A for 20 min (n = 5 per group). Illustrated CGRP concentrations show the evoked release minus the basal production in the same time in relation to total protein concentration of the DRG cell cultures. Although no significant differences in the release of CGRP between WT and IL-17KO were detectable, IL-17A (10 ng/ml) signalling increases CGRP release in WT DRG neurones (p = 0.045). *p

    Techniques Used: Isolation, Cell Culture, In Vitro, Mouse Assay, Protein Concentration

    12) Product Images from "Antibody blockade of IL-17 family cytokines in immunity to acute murine oral mucosal candidiasis"

    Article Title: Antibody blockade of IL-17 family cytokines in immunity to acute murine oral mucosal candidiasis

    Journal: Journal of Leukocyte Biology

    doi: 10.1189/jlb.4A0915-428R

    Anti-IL-17A antibodies but not anti-IL-17F antibodies render mice susceptible to OPC.
    Figure Legend Snippet: Anti-IL-17A antibodies but not anti-IL-17F antibodies render mice susceptible to OPC.

    Techniques Used: Mouse Assay

    13) Product Images from "Thrombospondin-1 Production Is Enhanced by Porphyromonas gingivalis Lipopolysaccharide in THP-1 Cells"

    Article Title: Thrombospondin-1 Production Is Enhanced by Porphyromonas gingivalis Lipopolysaccharide in THP-1 Cells

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0115107

    MG-132 inhibited TSP-1 mRNA expression in THP-1 cells. THP-1 cells were pretreated with 5.0 ng/ml of MG-132 (inhibitor of NF-κB) for 1 h, followed by the addition of 1.0 µg/ml of P. gingivalis LPS and 10 ng/ml of IL-17F. P. gingivalis LPS-induced TSP-1 mRNA was significantly reduced by MG-132. MG-132 also significantly reduced TSP-1 mRNA expression induced by P. gingivalis LPS together with IL-17F.
    Figure Legend Snippet: MG-132 inhibited TSP-1 mRNA expression in THP-1 cells. THP-1 cells were pretreated with 5.0 ng/ml of MG-132 (inhibitor of NF-κB) for 1 h, followed by the addition of 1.0 µg/ml of P. gingivalis LPS and 10 ng/ml of IL-17F. P. gingivalis LPS-induced TSP-1 mRNA was significantly reduced by MG-132. MG-132 also significantly reduced TSP-1 mRNA expression induced by P. gingivalis LPS together with IL-17F.

    Techniques Used: Expressing

    Effect of various cytokines on TSP-1 expression in THP-1 cells. THP-1 cells were co-stimulated with 1.0 µg/ml of P. gingivalis LPS and 10 ng/ml of each of IL-4, IL-17A, IL-17F, or IFN-γ for 4 h. TSP-1 mRNA expression was significantly enhanced by all co-stimulatory factors ( P
    Figure Legend Snippet: Effect of various cytokines on TSP-1 expression in THP-1 cells. THP-1 cells were co-stimulated with 1.0 µg/ml of P. gingivalis LPS and 10 ng/ml of each of IL-4, IL-17A, IL-17F, or IFN-γ for 4 h. TSP-1 mRNA expression was significantly enhanced by all co-stimulatory factors ( P

    Techniques Used: Expressing

    14) Product Images from "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 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

    Journal:

    doi:

    Effects of blocking IL-17R on GRO- α ( A ) and G-CSF ( B ) production by IL-17A and IL-17F. Primary HBE cells were pretreated with IL-17R Ab (2 μ g/ml) 30 min before IL-17A and IL-17F treatment (both at 10 ng/ml). Apical and basolateral medium
    Figure Legend Snippet: Effects of blocking IL-17R on GRO- α ( A ) and G-CSF ( B ) production by IL-17A and IL-17F. Primary HBE cells were pretreated with IL-17R Ab (2 μ g/ml) 30 min before IL-17A and IL-17F treatment (both at 10 ng/ml). Apical and basolateral medium

    Techniques Used: Blocking Assay

    GRO- α ( A ) and G-CSF ( B ) secreted after stimulation with IL-17F and/or TNF- α . primary HBE cells were treated with IL-17F (10 ng/ml) and TNF- α (1 ng/ml). The cytokine mixture (IL-17F + TNF- α ) was also preincubated with anti-IL-17
    Figure Legend Snippet: GRO- α ( A ) and G-CSF ( B ) secreted after stimulation with IL-17F and/or TNF- α . primary HBE cells were treated with IL-17F (10 ng/ml) and TNF- α (1 ng/ml). The cytokine mixture (IL-17F + TNF- α ) was also preincubated with anti-IL-17

    Techniques Used:

    Cytokines levels in sputum from CF patients undergoing pulmonary exacerbation. Panel A: IL-17A and IL-17F concentration in sputum from CF patients at different time points, as indicated, were measured by ELISA. Panel B: IL-17- induced cytokines IL-8 (upper
    Figure Legend Snippet: Cytokines levels in sputum from CF patients undergoing pulmonary exacerbation. Panel A: IL-17A and IL-17F concentration in sputum from CF patients at different time points, as indicated, were measured by ELISA. Panel B: IL-17- induced cytokines IL-8 (upper

    Techniques Used: Concentration Assay, Enzyme-linked Immunosorbent Assay

    A , Dose-dependent elevation of GRO- α , G-CSF, and MCP-1 protein levels by recombinant human IL-17A and IL-17F. Primary HBE cells were treated with different doses of IL-17A and IL-17F, as indicated. Basolateral media were collected 24 h after the
    Figure Legend Snippet: A , Dose-dependent elevation of GRO- α , G-CSF, and MCP-1 protein levels by recombinant human IL-17A and IL-17F. Primary HBE cells were treated with different doses of IL-17A and IL-17F, as indicated. Basolateral media were collected 24 h after the

    Techniques Used: Recombinant

    IL-17A and IL-17F up-regulate G-CSF, GRO-α, and MCP-1 in HBE cells: kinetic studies
    Figure Legend Snippet: IL-17A and IL-17F up-regulate G-CSF, GRO-α, and MCP-1 in HBE cells: kinetic studies

    Techniques Used:

    15) Product Images from "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 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

    Journal:

    doi:

    Effects of blocking IL-17R on GRO- α ( A ) and G-CSF ( B ) production by IL-17A and IL-17F. Primary HBE cells were pretreated with IL-17R Ab (2 μ g/ml) 30 min before IL-17A and IL-17F treatment (both at 10 ng/ml). Apical and basolateral medium
    Figure Legend Snippet: Effects of blocking IL-17R on GRO- α ( A ) and G-CSF ( B ) production by IL-17A and IL-17F. Primary HBE cells were pretreated with IL-17R Ab (2 μ g/ml) 30 min before IL-17A and IL-17F treatment (both at 10 ng/ml). Apical and basolateral medium

    Techniques Used: Blocking Assay

    GRO- α ( A ) and G-CSF ( B ) secreted after stimulation with IL-17F and/or TNF- α . primary HBE cells were treated with IL-17F (10 ng/ml) and TNF- α (1 ng/ml). The cytokine mixture (IL-17F + TNF- α ) was also preincubated with anti-IL-17
    Figure Legend Snippet: GRO- α ( A ) and G-CSF ( B ) secreted after stimulation with IL-17F and/or TNF- α . primary HBE cells were treated with IL-17F (10 ng/ml) and TNF- α (1 ng/ml). The cytokine mixture (IL-17F + TNF- α ) was also preincubated with anti-IL-17

    Techniques Used:

    Cytokines levels in sputum from CF patients undergoing pulmonary exacerbation. Panel A: IL-17A and IL-17F concentration in sputum from CF patients at different time points, as indicated, were measured by ELISA. Panel B: IL-17- induced cytokines IL-8 (upper
    Figure Legend Snippet: Cytokines levels in sputum from CF patients undergoing pulmonary exacerbation. Panel A: IL-17A and IL-17F concentration in sputum from CF patients at different time points, as indicated, were measured by ELISA. Panel B: IL-17- induced cytokines IL-8 (upper

    Techniques Used: Concentration Assay, Enzyme-linked Immunosorbent Assay

    A , Dose-dependent elevation of GRO- α , G-CSF, and MCP-1 protein levels by recombinant human IL-17A and IL-17F. Primary HBE cells were treated with different doses of IL-17A and IL-17F, as indicated. Basolateral media were collected 24 h after the
    Figure Legend Snippet: A , Dose-dependent elevation of GRO- α , G-CSF, and MCP-1 protein levels by recombinant human IL-17A and IL-17F. Primary HBE cells were treated with different doses of IL-17A and IL-17F, as indicated. Basolateral media were collected 24 h after the

    Techniques Used: Recombinant

    IL-17A and IL-17F up-regulate G-CSF, GRO-α, and MCP-1 in HBE cells: kinetic studies
    Figure Legend Snippet: IL-17A and IL-17F up-regulate G-CSF, GRO-α, and MCP-1 in HBE cells: kinetic studies

    Techniques Used:

    16) Product Images from "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 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

    Journal:

    doi:

    Effects of blocking IL-17R on GRO- α ( A ) and G-CSF ( B ) production by IL-17A and IL-17F. Primary HBE cells were pretreated with IL-17R Ab (2 μ g/ml) 30 min before IL-17A and IL-17F treatment (both at 10 ng/ml). Apical and basolateral medium
    Figure Legend Snippet: Effects of blocking IL-17R on GRO- α ( A ) and G-CSF ( B ) production by IL-17A and IL-17F. Primary HBE cells were pretreated with IL-17R Ab (2 μ g/ml) 30 min before IL-17A and IL-17F treatment (both at 10 ng/ml). Apical and basolateral medium

    Techniques Used: Blocking Assay

    GRO- α ( A ) and G-CSF ( B ) secreted after stimulation with IL-17F and/or TNF- α . primary HBE cells were treated with IL-17F (10 ng/ml) and TNF- α (1 ng/ml). The cytokine mixture (IL-17F + TNF- α ) was also preincubated with anti-IL-17
    Figure Legend Snippet: GRO- α ( A ) and G-CSF ( B ) secreted after stimulation with IL-17F and/or TNF- α . primary HBE cells were treated with IL-17F (10 ng/ml) and TNF- α (1 ng/ml). The cytokine mixture (IL-17F + TNF- α ) was also preincubated with anti-IL-17

    Techniques Used:

    Cytokines levels in sputum from CF patients undergoing pulmonary exacerbation. Panel A: IL-17A and IL-17F concentration in sputum from CF patients at different time points, as indicated, were measured by ELISA. Panel B: IL-17- induced cytokines IL-8 (upper
    Figure Legend Snippet: Cytokines levels in sputum from CF patients undergoing pulmonary exacerbation. Panel A: IL-17A and IL-17F concentration in sputum from CF patients at different time points, as indicated, were measured by ELISA. Panel B: IL-17- induced cytokines IL-8 (upper

    Techniques Used: Concentration Assay, Enzyme-linked Immunosorbent Assay

    A , Dose-dependent elevation of GRO- α , G-CSF, and MCP-1 protein levels by recombinant human IL-17A and IL-17F. Primary HBE cells were treated with different doses of IL-17A and IL-17F, as indicated. Basolateral media were collected 24 h after the
    Figure Legend Snippet: A , Dose-dependent elevation of GRO- α , G-CSF, and MCP-1 protein levels by recombinant human IL-17A and IL-17F. Primary HBE cells were treated with different doses of IL-17A and IL-17F, as indicated. Basolateral media were collected 24 h after the

    Techniques Used: Recombinant

    IL-17A and IL-17F up-regulate G-CSF, GRO-α, and MCP-1 in HBE cells: kinetic studies
    Figure Legend Snippet: IL-17A and IL-17F up-regulate G-CSF, GRO-α, and MCP-1 in HBE cells: kinetic studies

    Techniques Used:

    17) Product Images from "High IL-17E and Low IL-17C Dermal Expression Identifies a Fibrosis-Specific Motif Common to Morphea and Systemic Sclerosis"

    Article Title: High IL-17E and Low IL-17C Dermal Expression Identifies a Fibrosis-Specific Motif Common to Morphea and Systemic Sclerosis

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0105008

    IL-17A+ and IL-17F+ cell frequency positively correlates with disease duration. IL-17A+ and IL-17F+ cells were identified by immunohistochemistry. Each symbol represents a single individual. Significance was assessed by Pearson's correlation test. mo = months.
    Figure Legend Snippet: IL-17A+ and IL-17F+ cell frequency positively correlates with disease duration. IL-17A+ and IL-17F+ cells were identified by immunohistochemistry. Each symbol represents a single individual. Significance was assessed by Pearson's correlation test. mo = months.

    Techniques Used: Immunohistochemistry

    Frequency of IL-17A+ and IL-17F + cells in SSc and morphea. A. Immunohistochemical analysis of IL-17A and IL-17F in healthy (HD), lesional SSc and morphea skin. Arrows indicate IL-17A (upper panels) or IL-17F (lower panels) positive cells. Results are representative of 14 SSc, 5 Morphea and 8 HD individuals. Original magnification 20X, scale bar 100 µm. Insets, 2X. B. Frequency of IL-17A+ and IL-17F+ cells expressed as percentage of total cells. Each symbol represents a distinct individual and the line depicts the mean. Empty and full dots refer to limited and diffuse SSc, respectively. Significance was assessed by Mann-Whitney test.
    Figure Legend Snippet: Frequency of IL-17A+ and IL-17F + cells in SSc and morphea. A. Immunohistochemical analysis of IL-17A and IL-17F in healthy (HD), lesional SSc and morphea skin. Arrows indicate IL-17A (upper panels) or IL-17F (lower panels) positive cells. Results are representative of 14 SSc, 5 Morphea and 8 HD individuals. Original magnification 20X, scale bar 100 µm. Insets, 2X. B. Frequency of IL-17A+ and IL-17F+ cells expressed as percentage of total cells. Each symbol represents a distinct individual and the line depicts the mean. Empty and full dots refer to limited and diffuse SSc, respectively. Significance was assessed by Mann-Whitney test.

    Techniques Used: Immunohistochemistry, MANN-WHITNEY

    IL-17F and IL-17E, but not IL-17C, enhance MCP-1 and MMP-1 production by normal and SSc fibroblasts. Dermal fibroblasts were cultured in triplicate in the presence of increasing amounts (3, 30, 300, 600 ng/ml) of IL-17C, IL-17E or IL-17F for 48 h. Box-plot show the levels of MCP-1, IL-6, IL-8, MMP-1 and type I collagen assessed in fibroblast culture supernatants from 4 HD and 4 SSc. The box represents values between 25 th and 75 th percentile with a line at the median (50 th percentile). The whiskers extend above and below the box to show the highest and the lowest values. IL-17A (30 ng/ml), TNF (A, 1 ng/ml) or TGF-β (B, 10 ng/ml) were used as controls. Significance versus nil condition was assessed by one-sample t-test.
    Figure Legend Snippet: IL-17F and IL-17E, but not IL-17C, enhance MCP-1 and MMP-1 production by normal and SSc fibroblasts. Dermal fibroblasts were cultured in triplicate in the presence of increasing amounts (3, 30, 300, 600 ng/ml) of IL-17C, IL-17E or IL-17F for 48 h. Box-plot show the levels of MCP-1, IL-6, IL-8, MMP-1 and type I collagen assessed in fibroblast culture supernatants from 4 HD and 4 SSc. The box represents values between 25 th and 75 th percentile with a line at the median (50 th percentile). The whiskers extend above and below the box to show the highest and the lowest values. IL-17A (30 ng/ml), TNF (A, 1 ng/ml) or TGF-β (B, 10 ng/ml) were used as controls. Significance versus nil condition was assessed by one-sample t-test.

    Techniques Used: Cell Culture

    Co-expression of IL-17A with IL-17C or IL-17E. Indirect immunofluorescence analysis was used to assess the expression of IL-17A (green), in combination with IL-17C ( A ) or IL-17E ( B ) or IL-17F ( C ) (red), and DAPI staining for nuclei (blue) in the dermis of one biopsy of 3 assessed (1 HD, 1 SSc and 1 morphea). Original magnification 40X.
    Figure Legend Snippet: Co-expression of IL-17A with IL-17C or IL-17E. Indirect immunofluorescence analysis was used to assess the expression of IL-17A (green), in combination with IL-17C ( A ) or IL-17E ( B ) or IL-17F ( C ) (red), and DAPI staining for nuclei (blue) in the dermis of one biopsy of 3 assessed (1 HD, 1 SSc and 1 morphea). Original magnification 40X.

    Techniques Used: Expressing, Immunofluorescence, Staining

    18) Product Images from "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 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

    Journal:

    doi:

    Effects of blocking IL-17R on GRO- α ( A ) and G-CSF ( B ) production by IL-17A and IL-17F. Primary HBE cells were pretreated with IL-17R Ab (2 μ g/ml) 30 min before IL-17A and IL-17F treatment (both at 10 ng/ml). Apical and basolateral medium
    Figure Legend Snippet: Effects of blocking IL-17R on GRO- α ( A ) and G-CSF ( B ) production by IL-17A and IL-17F. Primary HBE cells were pretreated with IL-17R Ab (2 μ g/ml) 30 min before IL-17A and IL-17F treatment (both at 10 ng/ml). Apical and basolateral medium

    Techniques Used: Blocking Assay

    GRO- α ( A ) and G-CSF ( B ) secreted after stimulation with IL-17F and/or TNF- α . primary HBE cells were treated with IL-17F (10 ng/ml) and TNF- α (1 ng/ml). The cytokine mixture (IL-17F + TNF- α ) was also preincubated with anti-IL-17
    Figure Legend Snippet: GRO- α ( A ) and G-CSF ( B ) secreted after stimulation with IL-17F and/or TNF- α . primary HBE cells were treated with IL-17F (10 ng/ml) and TNF- α (1 ng/ml). The cytokine mixture (IL-17F + TNF- α ) was also preincubated with anti-IL-17

    Techniques Used:

    Cytokines levels in sputum from CF patients undergoing pulmonary exacerbation. Panel A: IL-17A and IL-17F concentration in sputum from CF patients at different time points, as indicated, were measured by ELISA. Panel B: IL-17- induced cytokines IL-8 (upper
    Figure Legend Snippet: Cytokines levels in sputum from CF patients undergoing pulmonary exacerbation. Panel A: IL-17A and IL-17F concentration in sputum from CF patients at different time points, as indicated, were measured by ELISA. Panel B: IL-17- induced cytokines IL-8 (upper

    Techniques Used: Concentration Assay, Enzyme-linked Immunosorbent Assay

    A , Dose-dependent elevation of GRO- α , G-CSF, and MCP-1 protein levels by recombinant human IL-17A and IL-17F. Primary HBE cells were treated with different doses of IL-17A and IL-17F, as indicated. Basolateral media were collected 24 h after the
    Figure Legend Snippet: A , Dose-dependent elevation of GRO- α , G-CSF, and MCP-1 protein levels by recombinant human IL-17A and IL-17F. Primary HBE cells were treated with different doses of IL-17A and IL-17F, as indicated. Basolateral media were collected 24 h after the

    Techniques Used: Recombinant

    IL-17A and IL-17F up-regulate G-CSF, GRO-α, and MCP-1 in HBE cells: kinetic studies
    Figure Legend Snippet: IL-17A and IL-17F up-regulate G-CSF, GRO-α, and MCP-1 in HBE cells: kinetic studies

    Techniques Used:

    19) Product Images from "IL‐17F induces IL‐6 via TAK1‐NFκB pathway in airway smooth muscle cells"

    Article Title: IL‐17F induces IL‐6 via TAK1‐NFκB pathway in airway smooth muscle cells

    Journal: Immunity, Inflammation and Disease

    doi: 10.1002/iid3.149

    Activation of NF‐κB by IL‐17F. (A) Kinetic activation of NF‐κB by IL‐17F in ASMCs. The cells were incubated with IL‐17F (100 ng/mL) for different time points as indicated. Western blotting was performed with Abs against total (t)‐p65 and phosphorylated (p)‐p65. (B) Effect of siRNAs targeting TAK1 on IL‐17F‐induced phosphorylation of p65. The cells were transfected with siRNAs targeting TAK1 or control siRNAs, and then ASMCs were stimulated with IL‐17F for 30 min. Western blotting analysis was performed with Abs against t‐p65 and p‐p65. The results shown are representative of three separate experiments.
    Figure Legend Snippet: Activation of NF‐κB by IL‐17F. (A) Kinetic activation of NF‐κB by IL‐17F in ASMCs. The cells were incubated with IL‐17F (100 ng/mL) for different time points as indicated. Western blotting was performed with Abs against total (t)‐p65 and phosphorylated (p)‐p65. (B) Effect of siRNAs targeting TAK1 on IL‐17F‐induced phosphorylation of p65. The cells were transfected with siRNAs targeting TAK1 or control siRNAs, and then ASMCs were stimulated with IL‐17F for 30 min. Western blotting analysis was performed with Abs against t‐p65 and p‐p65. The results shown are representative of three separate experiments.

    Techniques Used: Activation Assay, Incubation, Western Blot, Transfection

    The expression of IL‐6 gene and protein by IL‐17F in ASMCs. (A) Gene expression of IL‐6 by IL‐17F. Real‐time PCR was performed as described in Materials and Methods. ASMCs were stimulated with IL‐17F (100 ng/mL) for 4, 12, and 24 h (n = 6). * P
    Figure Legend Snippet: The expression of IL‐6 gene and protein by IL‐17F in ASMCs. (A) Gene expression of IL‐6 by IL‐17F. Real‐time PCR was performed as described in Materials and Methods. ASMCs were stimulated with IL‐17F (100 ng/mL) for 4, 12, and 24 h (n = 6). * P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction

    Activation of TAK1 by IL‐17F in ASMCs. The cells were incubated with IL‐17F (100 ng/mL) for different time points as indicated. Western blotting analysis was performed with Abs against total (t)‐TAK1 and phosphorylated (p)‐TAK1 as indicated. These results shown are representative of three separate experiments.
    Figure Legend Snippet: Activation of TAK1 by IL‐17F in ASMCs. The cells were incubated with IL‐17F (100 ng/mL) for different time points as indicated. Western blotting analysis was performed with Abs against total (t)‐TAK1 and phosphorylated (p)‐TAK1 as indicated. These results shown are representative of three separate experiments.

    Techniques Used: Activation Assay, Incubation, Western Blot

    Effect of NF‐κB inhibition on IL‐17F‐induced IL‐6 expression. (A) ASMCs were pretreated with NF‐κB inhibitor, BAY 11‐7082 for 1 h before the 24 h‐stimulation of IL‐17F (100 ng/mL), and then IL‐6 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM (n = 6). * P
    Figure Legend Snippet: Effect of NF‐κB inhibition on IL‐17F‐induced IL‐6 expression. (A) ASMCs were pretreated with NF‐κB inhibitor, BAY 11‐7082 for 1 h before the 24 h‐stimulation of IL‐17F (100 ng/mL), and then IL‐6 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM (n = 6). * P

    Techniques Used: Inhibition, Expressing, Enzyme-linked Immunosorbent Assay

    Effect of the inhibition for TAK1 on IL‐6 expression. ASMCs were pretreated with 5Z‐7‐Oxozeaenol (0.1, 0.5, and 1.0 µM) for 3 h before the 24 h‐stimulation of IL‐17F (100 ng/mL), and then IL‐6 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM (n = 6). * P
    Figure Legend Snippet: Effect of the inhibition for TAK1 on IL‐6 expression. ASMCs were pretreated with 5Z‐7‐Oxozeaenol (0.1, 0.5, and 1.0 µM) for 3 h before the 24 h‐stimulation of IL‐17F (100 ng/mL), and then IL‐6 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM (n = 6). * P

    Techniques Used: Inhibition, Expressing, Enzyme-linked Immunosorbent Assay

    20) Product Images from "IL‐17F induces IL‐6 via TAK1‐NFκB pathway in airway smooth muscle cells"

    Article Title: IL‐17F induces IL‐6 via TAK1‐NFκB pathway in airway smooth muscle cells

    Journal: Immunity, Inflammation and Disease

    doi: 10.1002/iid3.149

    Activation of NF‐κB by IL‐17F. (A) Kinetic activation of NF‐κB by IL‐17F in ASMCs. The cells were incubated with IL‐17F (100 ng/mL) for different time points as indicated. Western blotting was performed with Abs against total (t)‐p65 and phosphorylated (p)‐p65. (B) Effect of siRNAs targeting TAK1 on IL‐17F‐induced phosphorylation of p65. The cells were transfected with siRNAs targeting TAK1 or control siRNAs, and then ASMCs were stimulated with IL‐17F for 30 min. Western blotting analysis was performed with Abs against t‐p65 and p‐p65. The results shown are representative of three separate experiments.
    Figure Legend Snippet: Activation of NF‐κB by IL‐17F. (A) Kinetic activation of NF‐κB by IL‐17F in ASMCs. The cells were incubated with IL‐17F (100 ng/mL) for different time points as indicated. Western blotting was performed with Abs against total (t)‐p65 and phosphorylated (p)‐p65. (B) Effect of siRNAs targeting TAK1 on IL‐17F‐induced phosphorylation of p65. The cells were transfected with siRNAs targeting TAK1 or control siRNAs, and then ASMCs were stimulated with IL‐17F for 30 min. Western blotting analysis was performed with Abs against t‐p65 and p‐p65. The results shown are representative of three separate experiments.

    Techniques Used: Activation Assay, Incubation, Western Blot, Transfection

    The expression of IL‐6 gene and protein by IL‐17F in ASMCs. (A) Gene expression of IL‐6 by IL‐17F. Real‐time PCR was performed as described in Materials and Methods. ASMCs were stimulated with IL‐17F (100 ng/mL) for 4, 12, and 24 h (n = 6). * P
    Figure Legend Snippet: The expression of IL‐6 gene and protein by IL‐17F in ASMCs. (A) Gene expression of IL‐6 by IL‐17F. Real‐time PCR was performed as described in Materials and Methods. ASMCs were stimulated with IL‐17F (100 ng/mL) for 4, 12, and 24 h (n = 6). * P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction

    Activation of TAK1 by IL‐17F in ASMCs. The cells were incubated with IL‐17F (100 ng/mL) for different time points as indicated. Western blotting analysis was performed with Abs against total (t)‐TAK1 and phosphorylated (p)‐TAK1 as indicated. These results shown are representative of three separate experiments.
    Figure Legend Snippet: Activation of TAK1 by IL‐17F in ASMCs. The cells were incubated with IL‐17F (100 ng/mL) for different time points as indicated. Western blotting analysis was performed with Abs against total (t)‐TAK1 and phosphorylated (p)‐TAK1 as indicated. These results shown are representative of three separate experiments.

    Techniques Used: Activation Assay, Incubation, Western Blot

    Effect of NF‐κB inhibition on IL‐17F‐induced IL‐6 expression. (A) ASMCs were pretreated with NF‐κB inhibitor, BAY 11‐7082 for 1 h before the 24 h‐stimulation of IL‐17F (100 ng/mL), and then IL‐6 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM (n = 6). * P
    Figure Legend Snippet: Effect of NF‐κB inhibition on IL‐17F‐induced IL‐6 expression. (A) ASMCs were pretreated with NF‐κB inhibitor, BAY 11‐7082 for 1 h before the 24 h‐stimulation of IL‐17F (100 ng/mL), and then IL‐6 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM (n = 6). * P

    Techniques Used: Inhibition, Expressing, Enzyme-linked Immunosorbent Assay

    Effect of the inhibition for TAK1 on IL‐6 expression. ASMCs were pretreated with 5Z‐7‐Oxozeaenol (0.1, 0.5, and 1.0 µM) for 3 h before the 24 h‐stimulation of IL‐17F (100 ng/mL), and then IL‐6 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM (n = 6). * P
    Figure Legend Snippet: Effect of the inhibition for TAK1 on IL‐6 expression. ASMCs were pretreated with 5Z‐7‐Oxozeaenol (0.1, 0.5, and 1.0 µM) for 3 h before the 24 h‐stimulation of IL‐17F (100 ng/mL), and then IL‐6 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM (n = 6). * P

    Techniques Used: Inhibition, Expressing, Enzyme-linked Immunosorbent Assay

    21) Product Images from "IL-17F Induces CCL20 in Bronchial Epithelial Cells"

    Article Title: IL-17F Induces CCL20 in Bronchial Epithelial Cells

    Journal: Journal of Allergy

    doi: 10.1155/2011/587204

    Effect of overexpression of dominant-negative mutants Raf1 and Ras on CCL20 protein expression in BEAS-2B cells. The cells overexpressing dominant-negative mutants were stimulated with IL-17F for 24 hrs, and CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P
    Figure Legend Snippet: Effect of overexpression of dominant-negative mutants Raf1 and Ras on CCL20 protein expression in BEAS-2B cells. The cells overexpressing dominant-negative mutants were stimulated with IL-17F for 24 hrs, and CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P

    Techniques Used: Over Expression, Dominant Negative Mutation, Expressing, Enzyme-linked Immunosorbent Assay

    Effect of MSK1 inhibitors, H89, and Ro318220 on IL-17F-induced CCL20. BEAS-2B cells were pretreated for 1 hr as indicated before the 24-hr stimulation of IL-17F, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P
    Figure Legend Snippet: Effect of MSK1 inhibitors, H89, and Ro318220 on IL-17F-induced CCL20. BEAS-2B cells were pretreated for 1 hr as indicated before the 24-hr stimulation of IL-17F, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P

    Techniques Used: Enzyme-linked Immunosorbent Assay

    Effect of siRNA for p90RSK, MSK1 and CREB on IL-17F-induced CCL20 expression. BEAS-2B cells transfected with siRNAs as indicated were stimulated with IL-17F for 24 hrs, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as mean s ± SEM ( n = 6). * P
    Figure Legend Snippet: Effect of siRNA for p90RSK, MSK1 and CREB on IL-17F-induced CCL20 expression. BEAS-2B cells transfected with siRNAs as indicated were stimulated with IL-17F for 24 hrs, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as mean s ± SEM ( n = 6). * P

    Techniques Used: Expressing, Transfection, Enzyme-linked Immunosorbent Assay

    The expression of CCL20 gene and protein by IL-17F in bronchial epithelial cells. (a) CCL20 gene expression by real-time PCR in BEAS-2B cells. Real-time PCR was performed as described in Materials and Methods. BEAS-2B cells were stimulated with IL-17F for 4 hrs ( n = 6). (c) CCL20 protein levels in supernatants in BEAS-2B cells. ELISA was performed ( n = 6). (d) CCL20 protein levels in supernatants in NHBEs ( n = 6). * P
    Figure Legend Snippet: The expression of CCL20 gene and protein by IL-17F in bronchial epithelial cells. (a) CCL20 gene expression by real-time PCR in BEAS-2B cells. Real-time PCR was performed as described in Materials and Methods. BEAS-2B cells were stimulated with IL-17F for 4 hrs ( n = 6). (c) CCL20 protein levels in supernatants in BEAS-2B cells. ELISA was performed ( n = 6). (d) CCL20 protein levels in supernatants in NHBEs ( n = 6). * P

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

    Effect of PD98059 (PD), U0126, Raf1 kinase inhibitor I (Raf I), SB202190 (SB), and SP600125 (SP) on CCL20 protein expression in BEAS-2Bs. The cells were pretreated for 1 hr as indicated before the 24-hr stimulation of IL-17F, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P
    Figure Legend Snippet: Effect of PD98059 (PD), U0126, Raf1 kinase inhibitor I (Raf I), SB202190 (SB), and SP600125 (SP) on CCL20 protein expression in BEAS-2Bs. The cells were pretreated for 1 hr as indicated before the 24-hr stimulation of IL-17F, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P

    Techniques Used: Expressing, Enzyme-linked Immunosorbent Assay

    22) Product Images from "IL-17F Induces CCL20 in Bronchial Epithelial Cells"

    Article Title: IL-17F Induces CCL20 in Bronchial Epithelial Cells

    Journal: Journal of Allergy

    doi: 10.1155/2011/587204

    Effect of overexpression of dominant-negative mutants Raf1 and Ras on CCL20 protein expression in BEAS-2B cells. The cells overexpressing dominant-negative mutants were stimulated with IL-17F for 24 hrs, and CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P
    Figure Legend Snippet: Effect of overexpression of dominant-negative mutants Raf1 and Ras on CCL20 protein expression in BEAS-2B cells. The cells overexpressing dominant-negative mutants were stimulated with IL-17F for 24 hrs, and CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P

    Techniques Used: Over Expression, Dominant Negative Mutation, Expressing, Enzyme-linked Immunosorbent Assay

    Effect of MSK1 inhibitors, H89, and Ro318220 on IL-17F-induced CCL20. BEAS-2B cells were pretreated for 1 hr as indicated before the 24-hr stimulation of IL-17F, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P
    Figure Legend Snippet: Effect of MSK1 inhibitors, H89, and Ro318220 on IL-17F-induced CCL20. BEAS-2B cells were pretreated for 1 hr as indicated before the 24-hr stimulation of IL-17F, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P

    Techniques Used: Enzyme-linked Immunosorbent Assay

    Effect of siRNA for p90RSK, MSK1 and CREB on IL-17F-induced CCL20 expression. BEAS-2B cells transfected with siRNAs as indicated were stimulated with IL-17F for 24 hrs, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as mean s ± SEM ( n = 6). * P
    Figure Legend Snippet: Effect of siRNA for p90RSK, MSK1 and CREB on IL-17F-induced CCL20 expression. BEAS-2B cells transfected with siRNAs as indicated were stimulated with IL-17F for 24 hrs, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as mean s ± SEM ( n = 6). * P

    Techniques Used: Expressing, Transfection, Enzyme-linked Immunosorbent Assay

    The expression of CCL20 gene and protein by IL-17F in bronchial epithelial cells. (a) CCL20 gene expression by real-time PCR in BEAS-2B cells. Real-time PCR was performed as described in Materials and Methods. BEAS-2B cells were stimulated with IL-17F for 4 hrs ( n = 6). (c) CCL20 protein levels in supernatants in BEAS-2B cells. ELISA was performed ( n = 6). (d) CCL20 protein levels in supernatants in NHBEs ( n = 6). * P
    Figure Legend Snippet: The expression of CCL20 gene and protein by IL-17F in bronchial epithelial cells. (a) CCL20 gene expression by real-time PCR in BEAS-2B cells. Real-time PCR was performed as described in Materials and Methods. BEAS-2B cells were stimulated with IL-17F for 4 hrs ( n = 6). (c) CCL20 protein levels in supernatants in BEAS-2B cells. ELISA was performed ( n = 6). (d) CCL20 protein levels in supernatants in NHBEs ( n = 6). * P

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

    Effect of PD98059 (PD), U0126, Raf1 kinase inhibitor I (Raf I), SB202190 (SB), and SP600125 (SP) on CCL20 protein expression in BEAS-2Bs. The cells were pretreated for 1 hr as indicated before the 24-hr stimulation of IL-17F, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P
    Figure Legend Snippet: Effect of PD98059 (PD), U0126, Raf1 kinase inhibitor I (Raf I), SB202190 (SB), and SP600125 (SP) on CCL20 protein expression in BEAS-2Bs. The cells were pretreated for 1 hr as indicated before the 24-hr stimulation of IL-17F, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P

    Techniques Used: Expressing, Enzyme-linked Immunosorbent Assay

    23) Product Images from "IL-17F Induces CCL20 in Bronchial Epithelial Cells"

    Article Title: IL-17F Induces CCL20 in Bronchial Epithelial Cells

    Journal: Journal of Allergy

    doi: 10.1155/2011/587204

    Effect of overexpression of dominant-negative mutants Raf1 and Ras on CCL20 protein expression in BEAS-2B cells. The cells overexpressing dominant-negative mutants were stimulated with IL-17F for 24 hrs, and CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P
    Figure Legend Snippet: Effect of overexpression of dominant-negative mutants Raf1 and Ras on CCL20 protein expression in BEAS-2B cells. The cells overexpressing dominant-negative mutants were stimulated with IL-17F for 24 hrs, and CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P

    Techniques Used: Over Expression, Dominant Negative Mutation, Expressing, Enzyme-linked Immunosorbent Assay

    Effect of MSK1 inhibitors, H89, and Ro318220 on IL-17F-induced CCL20. BEAS-2B cells were pretreated for 1 hr as indicated before the 24-hr stimulation of IL-17F, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P
    Figure Legend Snippet: Effect of MSK1 inhibitors, H89, and Ro318220 on IL-17F-induced CCL20. BEAS-2B cells were pretreated for 1 hr as indicated before the 24-hr stimulation of IL-17F, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P

    Techniques Used: Enzyme-linked Immunosorbent Assay

    Effect of siRNA for p90RSK, MSK1 and CREB on IL-17F-induced CCL20 expression. BEAS-2B cells transfected with siRNAs as indicated were stimulated with IL-17F for 24 hrs, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as mean s ± SEM ( n = 6). * P
    Figure Legend Snippet: Effect of siRNA for p90RSK, MSK1 and CREB on IL-17F-induced CCL20 expression. BEAS-2B cells transfected with siRNAs as indicated were stimulated with IL-17F for 24 hrs, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as mean s ± SEM ( n = 6). * P

    Techniques Used: Expressing, Transfection, Enzyme-linked Immunosorbent Assay

    The expression of CCL20 gene and protein by IL-17F in bronchial epithelial cells. (a) CCL20 gene expression by real-time PCR in BEAS-2B cells. Real-time PCR was performed as described in Materials and Methods. BEAS-2B cells were stimulated with IL-17F for 4 hrs ( n = 6). (c) CCL20 protein levels in supernatants in BEAS-2B cells. ELISA was performed ( n = 6). (d) CCL20 protein levels in supernatants in NHBEs ( n = 6). * P
    Figure Legend Snippet: The expression of CCL20 gene and protein by IL-17F in bronchial epithelial cells. (a) CCL20 gene expression by real-time PCR in BEAS-2B cells. Real-time PCR was performed as described in Materials and Methods. BEAS-2B cells were stimulated with IL-17F for 4 hrs ( n = 6). (c) CCL20 protein levels in supernatants in BEAS-2B cells. ELISA was performed ( n = 6). (d) CCL20 protein levels in supernatants in NHBEs ( n = 6). * P

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

    Effect of PD98059 (PD), U0126, Raf1 kinase inhibitor I (Raf I), SB202190 (SB), and SP600125 (SP) on CCL20 protein expression in BEAS-2Bs. The cells were pretreated for 1 hr as indicated before the 24-hr stimulation of IL-17F, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P
    Figure Legend Snippet: Effect of PD98059 (PD), U0126, Raf1 kinase inhibitor I (Raf I), SB202190 (SB), and SP600125 (SP) on CCL20 protein expression in BEAS-2Bs. The cells were pretreated for 1 hr as indicated before the 24-hr stimulation of IL-17F, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P

    Techniques Used: Expressing, Enzyme-linked Immunosorbent Assay

    24) Product Images from "Expression of the T Helper 17-Associated Cytokines IL-17A and IL-17F in Asthma and COPD"

    Article Title: Expression of the T Helper 17-Associated Cytokines IL-17A and IL-17F in Asthma and COPD

    Journal: Chest

    doi: 10.1378/chest.09-3058

    IL-17A and IL-17F expression in the submucosa in COPD. Representative photomicrographs of proximal airway resections from COPD tissue, illustrating isotype control. A, Goat IgG. B, IL-17A + cells present in the submucosa. C, IL-17F + cells in the submucosa (× 400). IL-17A/F + cells highlighted by arrows. D, The number of IL-17A + and E, IL-17F + cells in the submucosa of healthy control subjects (never smokers), healthy control subjects (smokers), and subjects with COPD. P values for across-group comparison by Kruskal-Wallis test and Dunn post hoc test for between-group comparisons are as shown.
    Figure Legend Snippet: IL-17A and IL-17F expression in the submucosa in COPD. Representative photomicrographs of proximal airway resections from COPD tissue, illustrating isotype control. A, Goat IgG. B, IL-17A + cells present in the submucosa. C, IL-17F + cells in the submucosa (× 400). IL-17A/F + cells highlighted by arrows. D, The number of IL-17A + and E, IL-17F + cells in the submucosa of healthy control subjects (never smokers), healthy control subjects (smokers), and subjects with COPD. P values for across-group comparison by Kruskal-Wallis test and Dunn post hoc test for between-group comparisons are as shown.

    Techniques Used: Expressing

    IL-17A and IL-17F expression in the submucosa in asthma. Representative photomicrographs of bronchial biopsy sections from subjects with severe asthma, illustrating isotype control. A, Goat IgG. B, IL-17A + cells present in the bronchial submucosa. C, IL-17F + cells in the submucosa (× 400). IL-17A/F + cells highlighted by arrows. D, The number of IL-17A + and E, IL-17F + cells in the bronchial submucosa of healthy control subjects, subjects with mild to moderate asthma (Global Initiative for Asthma [GINA] 1-3), and subjects with severe asthma (GINA 4-5). P values for across-group comparison by Kruskal-Wallis test and Dunn post hoc test for between-group comparisons are as shown.
    Figure Legend Snippet: IL-17A and IL-17F expression in the submucosa in asthma. Representative photomicrographs of bronchial biopsy sections from subjects with severe asthma, illustrating isotype control. A, Goat IgG. B, IL-17A + cells present in the bronchial submucosa. C, IL-17F + cells in the submucosa (× 400). IL-17A/F + cells highlighted by arrows. D, The number of IL-17A + and E, IL-17F + cells in the bronchial submucosa of healthy control subjects, subjects with mild to moderate asthma (Global Initiative for Asthma [GINA] 1-3), and subjects with severe asthma (GINA 4-5). P values for across-group comparison by Kruskal-Wallis test and Dunn post hoc test for between-group comparisons are as shown.

    Techniques Used: Expressing

    25) Product Images from "Effect of 12-O-tetradecanoylphorbol-13-acetate-induced psoriasis-like skin lesions on systemic inflammation and atherosclerosis in hypercholesterolaemic apolipoprotein E deficient mice"

    Article Title: Effect of 12-O-tetradecanoylphorbol-13-acetate-induced psoriasis-like skin lesions on systemic inflammation and atherosclerosis in hypercholesterolaemic apolipoprotein E deficient mice

    Journal: BMC Dermatology

    doi: 10.1186/s12895-016-0046-1

    Topical 12- O -tetradecanoylphorbol-13-acetate (TPA) induces local skin inflammation with increased skin thickness and interleukin (IL)-17F levels. a Representative photos illustrating the red and scaly appearance of ears after TPA application as compared to control ears, and representative hematoxylin and eosin-stained ear cross-sections at 10× magnification. Scale bar = 200 μm. TPA led to epidermal hyperproliferation ( star ) and dermal inflammation ( arrow ). b Ear thickness (mm) was measured twice weekly in ApoE −/− mice after TPA or vehicle application. Data from two separate, but similar studies with vehicle or TPA application on both ears were included; study 1: n = 5–7/group ( unfilled circle: control, filled circle : TPA), study 2: n = 15/group ( unfilled triangle: control, filled triangle : TPA). The depicted values in b are mean ± SD, i.e., mean value of right and left ear for each mouse. p
    Figure Legend Snippet: Topical 12- O -tetradecanoylphorbol-13-acetate (TPA) induces local skin inflammation with increased skin thickness and interleukin (IL)-17F levels. a Representative photos illustrating the red and scaly appearance of ears after TPA application as compared to control ears, and representative hematoxylin and eosin-stained ear cross-sections at 10× magnification. Scale bar = 200 μm. TPA led to epidermal hyperproliferation ( star ) and dermal inflammation ( arrow ). b Ear thickness (mm) was measured twice weekly in ApoE −/− mice after TPA or vehicle application. Data from two separate, but similar studies with vehicle or TPA application on both ears were included; study 1: n = 5–7/group ( unfilled circle: control, filled circle : TPA), study 2: n = 15/group ( unfilled triangle: control, filled triangle : TPA). The depicted values in b are mean ± SD, i.e., mean value of right and left ear for each mouse. p

    Techniques Used: Staining, Mouse Assay

    26) Product Images from "Aggravated Atherosclerosis and Vascular Inflammation With Reduced Kidney Function Depend on Interleukin-17 Receptor A and Are Normalized by Inhibition of Interleukin-17A"

    Article Title: Aggravated Atherosclerosis and Vascular Inflammation With Reduced Kidney Function Depend on Interleukin-17 Receptor A and Are Normalized by Inhibition of Interleukin-17A

    Journal: JACC: Basic to Translational Science

    doi: 10.1016/j.jacbts.2017.08.005

    IL-17A Promotes Inflammatory Cytokine Expression in Endothelial Cells (A) IL-17 receptor A ( Il17ra ) and auxiliary subunits Il17rc and Il17re mRNA expression was determined by using quantitative polymerase chain reaction (qPCR). Il17rb messenger ribonucleic acid (mRNA) was below detection limit (n = 4, 2 exp.). (B to I) Endothelial cells were stimulated for 2 h with 50 ng/ml IL-17A (B to E) or IL-17F (F to I) . CCL2 (B and F) , CXCL1 (C and G) , IL-6 (D and H) , and granulocyte-macrophage colony-stimulating factor (GM-CSF) (E and I) cytokine expression quantified by using qPCR (n = 8 from 4 independent experiments for each cytokine).
    Figure Legend Snippet: IL-17A Promotes Inflammatory Cytokine Expression in Endothelial Cells (A) IL-17 receptor A ( Il17ra ) and auxiliary subunits Il17rc and Il17re mRNA expression was determined by using quantitative polymerase chain reaction (qPCR). Il17rb messenger ribonucleic acid (mRNA) was below detection limit (n = 4, 2 exp.). (B to I) Endothelial cells were stimulated for 2 h with 50 ng/ml IL-17A (B to E) or IL-17F (F to I) . CCL2 (B and F) , CXCL1 (C and G) , IL-6 (D and H) , and granulocyte-macrophage colony-stimulating factor (GM-CSF) (E and I) cytokine expression quantified by using qPCR (n = 8 from 4 independent experiments for each cytokine).

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction

    27) Product Images from "Aggravated Atherosclerosis and Vascular Inflammation With Reduced Kidney Function Depend on Interleukin-17 Receptor A and Are Normalized by Inhibition of Interleukin-17A"

    Article Title: Aggravated Atherosclerosis and Vascular Inflammation With Reduced Kidney Function Depend on Interleukin-17 Receptor A and Are Normalized by Inhibition of Interleukin-17A

    Journal: JACC: Basic to Translational Science

    doi: 10.1016/j.jacbts.2017.08.005

    IL-17A Promotes Inflammatory Cytokine Expression in Endothelial Cells (A) IL-17 receptor A ( Il17ra ) and auxiliary subunits Il17rc and Il17re mRNA expression was determined by using quantitative polymerase chain reaction (qPCR). Il17rb messenger ribonucleic acid (mRNA) was below detection limit (n = 4, 2 exp.). (B to I) Endothelial cells were stimulated for 2 h with 50 ng/ml IL-17A (B to E) or IL-17F (F to I) . CCL2 (B and F) , CXCL1 (C and G) , IL-6 (D and H) , and granulocyte-macrophage colony-stimulating factor (GM-CSF) (E and I) cytokine expression quantified by using qPCR (n = 8 from 4 independent experiments for each cytokine).
    Figure Legend Snippet: IL-17A Promotes Inflammatory Cytokine Expression in Endothelial Cells (A) IL-17 receptor A ( Il17ra ) and auxiliary subunits Il17rc and Il17re mRNA expression was determined by using quantitative polymerase chain reaction (qPCR). Il17rb messenger ribonucleic acid (mRNA) was below detection limit (n = 4, 2 exp.). (B to I) Endothelial cells were stimulated for 2 h with 50 ng/ml IL-17A (B to E) or IL-17F (F to I) . CCL2 (B and F) , CXCL1 (C and G) , IL-6 (D and H) , and granulocyte-macrophage colony-stimulating factor (GM-CSF) (E and I) cytokine expression quantified by using qPCR (n = 8 from 4 independent experiments for each cytokine).

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction

    28) Product Images from "Epithelial TRAF6 drives IL-17–mediated psoriatic inflammation"

    Article Title: Epithelial TRAF6 drives IL-17–mediated psoriatic inflammation

    Journal: JCI Insight

    doi: 10.1172/jci.insight.121175

    IMQ enhanced psoriasis-related gene expression in keratinocytes via TRAF6-dependent signaling pathway. ( A ) Western blot analysis of keratinocytes from Traf6EKO mice and Traf6 fl/fl mice stimulated with rIL-1β at the indicated time points. Total cell lysates were resolved by SDS-PAGE followed by immunoblotting. ( B ) qPCR analysis of mRNA levels in the primary cultured keratinocytes from Traf6EKO mice and Traf6 fl/fl mice stimulated with IMQ for 0–6 hours ( n = 3). ( C and D ) qPCR analysis of mRNA levels in the primary cultured keratinocytes from Traf6EKO mice and Traf6 fl/fl mice treated with IL-17A (100 ng/ml) ( C ) and IL-17F (100 ng/ml) ( D ) for 0–6 hours ( n = 3). These results were normalized to Gapdh expression and are shown as means ± SD. * P
    Figure Legend Snippet: IMQ enhanced psoriasis-related gene expression in keratinocytes via TRAF6-dependent signaling pathway. ( A ) Western blot analysis of keratinocytes from Traf6EKO mice and Traf6 fl/fl mice stimulated with rIL-1β at the indicated time points. Total cell lysates were resolved by SDS-PAGE followed by immunoblotting. ( B ) qPCR analysis of mRNA levels in the primary cultured keratinocytes from Traf6EKO mice and Traf6 fl/fl mice stimulated with IMQ for 0–6 hours ( n = 3). ( C and D ) qPCR analysis of mRNA levels in the primary cultured keratinocytes from Traf6EKO mice and Traf6 fl/fl mice treated with IL-17A (100 ng/ml) ( C ) and IL-17F (100 ng/ml) ( D ) for 0–6 hours ( n = 3). These results were normalized to Gapdh expression and are shown as means ± SD. * P

    Techniques Used: Expressing, Western Blot, Mouse Assay, SDS Page, Real-time Polymerase Chain Reaction, Cell Culture

    29) Product Images from "Antibody blockade of IL-17 family cytokines in immunity to acute murine oral mucosal candidiasis"

    Article Title: Antibody blockade of IL-17 family cytokines in immunity to acute murine oral mucosal candidiasis

    Journal: Journal of Leukocyte Biology

    doi: 10.1189/jlb.4A0915-428R

    Anti-IL-17A antibodies but not anti-IL-17F antibodies render mice susceptible to OPC.
    Figure Legend Snippet: Anti-IL-17A antibodies but not anti-IL-17F antibodies render mice susceptible to OPC.

    Techniques Used: Mouse Assay

    30) Product Images from "IL‐17F induces IL‐6 via TAK1‐NFκB pathway in airway smooth muscle cells"

    Article Title: IL‐17F induces IL‐6 via TAK1‐NFκB pathway in airway smooth muscle cells

    Journal: Immunity, Inflammation and Disease

    doi: 10.1002/iid3.149

    Activation of NF‐κB by IL‐17F. (A) Kinetic activation of NF‐κB by IL‐17F in ASMCs. The cells were incubated with IL‐17F (100 ng/mL) for different time points as indicated. Western blotting was performed with Abs against total (t)‐p65 and phosphorylated (p)‐p65. (B) Effect of siRNAs targeting TAK1 on IL‐17F‐induced phosphorylation of p65. The cells were transfected with siRNAs targeting TAK1 or control siRNAs, and then ASMCs were stimulated with IL‐17F for 30 min. Western blotting analysis was performed with Abs against t‐p65 and p‐p65. The results shown are representative of three separate experiments.
    Figure Legend Snippet: Activation of NF‐κB by IL‐17F. (A) Kinetic activation of NF‐κB by IL‐17F in ASMCs. The cells were incubated with IL‐17F (100 ng/mL) for different time points as indicated. Western blotting was performed with Abs against total (t)‐p65 and phosphorylated (p)‐p65. (B) Effect of siRNAs targeting TAK1 on IL‐17F‐induced phosphorylation of p65. The cells were transfected with siRNAs targeting TAK1 or control siRNAs, and then ASMCs were stimulated with IL‐17F for 30 min. Western blotting analysis was performed with Abs against t‐p65 and p‐p65. The results shown are representative of three separate experiments.

    Techniques Used: Activation Assay, Incubation, Western Blot, Transfection

    The expression of IL‐6 gene and protein by IL‐17F in ASMCs. (A) Gene expression of IL‐6 by IL‐17F. Real‐time PCR was performed as described in Materials and Methods. ASMCs were stimulated with IL‐17F (100 ng/mL) for 4, 12, and 24 h (n = 6). * P
    Figure Legend Snippet: The expression of IL‐6 gene and protein by IL‐17F in ASMCs. (A) Gene expression of IL‐6 by IL‐17F. Real‐time PCR was performed as described in Materials and Methods. ASMCs were stimulated with IL‐17F (100 ng/mL) for 4, 12, and 24 h (n = 6). * P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction

    Activation of TAK1 by IL‐17F in ASMCs. The cells were incubated with IL‐17F (100 ng/mL) for different time points as indicated. Western blotting analysis was performed with Abs against total (t)‐TAK1 and phosphorylated (p)‐TAK1 as indicated. These results shown are representative of three separate experiments.
    Figure Legend Snippet: Activation of TAK1 by IL‐17F in ASMCs. The cells were incubated with IL‐17F (100 ng/mL) for different time points as indicated. Western blotting analysis was performed with Abs against total (t)‐TAK1 and phosphorylated (p)‐TAK1 as indicated. These results shown are representative of three separate experiments.

    Techniques Used: Activation Assay, Incubation, Western Blot

    Effect of NF‐κB inhibition on IL‐17F‐induced IL‐6 expression. (A) ASMCs were pretreated with NF‐κB inhibitor, BAY 11‐7082 for 1 h before the 24 h‐stimulation of IL‐17F (100 ng/mL), and then IL‐6 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM (n = 6). * P
    Figure Legend Snippet: Effect of NF‐κB inhibition on IL‐17F‐induced IL‐6 expression. (A) ASMCs were pretreated with NF‐κB inhibitor, BAY 11‐7082 for 1 h before the 24 h‐stimulation of IL‐17F (100 ng/mL), and then IL‐6 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM (n = 6). * P

    Techniques Used: Inhibition, Expressing, Enzyme-linked Immunosorbent Assay

    Effect of the inhibition for TAK1 on IL‐6 expression. ASMCs were pretreated with 5Z‐7‐Oxozeaenol (0.1, 0.5, and 1.0 µM) for 3 h before the 24 h‐stimulation of IL‐17F (100 ng/mL), and then IL‐6 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM (n = 6). * P
    Figure Legend Snippet: Effect of the inhibition for TAK1 on IL‐6 expression. ASMCs were pretreated with 5Z‐7‐Oxozeaenol (0.1, 0.5, and 1.0 µM) for 3 h before the 24 h‐stimulation of IL‐17F (100 ng/mL), and then IL‐6 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM (n = 6). * P

    Techniques Used: Inhibition, Expressing, Enzyme-linked Immunosorbent Assay

    31) Product Images from "IL‐17F induces IL‐6 via TAK1‐NFκB pathway in airway smooth muscle cells"

    Article Title: IL‐17F induces IL‐6 via TAK1‐NFκB pathway in airway smooth muscle cells

    Journal: Immunity, Inflammation and Disease

    doi: 10.1002/iid3.149

    Activation of NF‐κB by IL‐17F. (A) Kinetic activation of NF‐κB by IL‐17F in ASMCs. The cells were incubated with IL‐17F (100 ng/mL) for different time points as indicated. Western blotting was performed with Abs against total (t)‐p65 and phosphorylated (p)‐p65. (B) Effect of siRNAs targeting TAK1 on IL‐17F‐induced phosphorylation of p65. The cells were transfected with siRNAs targeting TAK1 or control siRNAs, and then ASMCs were stimulated with IL‐17F for 30 min. Western blotting analysis was performed with Abs against t‐p65 and p‐p65. The results shown are representative of three separate experiments.
    Figure Legend Snippet: Activation of NF‐κB by IL‐17F. (A) Kinetic activation of NF‐κB by IL‐17F in ASMCs. The cells were incubated with IL‐17F (100 ng/mL) for different time points as indicated. Western blotting was performed with Abs against total (t)‐p65 and phosphorylated (p)‐p65. (B) Effect of siRNAs targeting TAK1 on IL‐17F‐induced phosphorylation of p65. The cells were transfected with siRNAs targeting TAK1 or control siRNAs, and then ASMCs were stimulated with IL‐17F for 30 min. Western blotting analysis was performed with Abs against t‐p65 and p‐p65. The results shown are representative of three separate experiments.

    Techniques Used: Activation Assay, Incubation, Western Blot, Transfection

    The expression of IL‐6 gene and protein by IL‐17F in ASMCs. (A) Gene expression of IL‐6 by IL‐17F. Real‐time PCR was performed as described in Materials and Methods. ASMCs were stimulated with IL‐17F (100 ng/mL) for 4, 12, and 24 h (n = 6). * P
    Figure Legend Snippet: The expression of IL‐6 gene and protein by IL‐17F in ASMCs. (A) Gene expression of IL‐6 by IL‐17F. Real‐time PCR was performed as described in Materials and Methods. ASMCs were stimulated with IL‐17F (100 ng/mL) for 4, 12, and 24 h (n = 6). * P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction

    Activation of TAK1 by IL‐17F in ASMCs. The cells were incubated with IL‐17F (100 ng/mL) for different time points as indicated. Western blotting analysis was performed with Abs against total (t)‐TAK1 and phosphorylated (p)‐TAK1 as indicated. These results shown are representative of three separate experiments.
    Figure Legend Snippet: Activation of TAK1 by IL‐17F in ASMCs. The cells were incubated with IL‐17F (100 ng/mL) for different time points as indicated. Western blotting analysis was performed with Abs against total (t)‐TAK1 and phosphorylated (p)‐TAK1 as indicated. These results shown are representative of three separate experiments.

    Techniques Used: Activation Assay, Incubation, Western Blot

    Effect of NF‐κB inhibition on IL‐17F‐induced IL‐6 expression. (A) ASMCs were pretreated with NF‐κB inhibitor, BAY 11‐7082 for 1 h before the 24 h‐stimulation of IL‐17F (100 ng/mL), and then IL‐6 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM (n = 6). * P
    Figure Legend Snippet: Effect of NF‐κB inhibition on IL‐17F‐induced IL‐6 expression. (A) ASMCs were pretreated with NF‐κB inhibitor, BAY 11‐7082 for 1 h before the 24 h‐stimulation of IL‐17F (100 ng/mL), and then IL‐6 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM (n = 6). * P

    Techniques Used: Inhibition, Expressing, Enzyme-linked Immunosorbent Assay

    Effect of the inhibition for TAK1 on IL‐6 expression. ASMCs were pretreated with 5Z‐7‐Oxozeaenol (0.1, 0.5, and 1.0 µM) for 3 h before the 24 h‐stimulation of IL‐17F (100 ng/mL), and then IL‐6 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM (n = 6). * P
    Figure Legend Snippet: Effect of the inhibition for TAK1 on IL‐6 expression. ASMCs were pretreated with 5Z‐7‐Oxozeaenol (0.1, 0.5, and 1.0 µM) for 3 h before the 24 h‐stimulation of IL‐17F (100 ng/mL), and then IL‐6 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM (n = 6). * P

    Techniques Used: Inhibition, Expressing, Enzyme-linked Immunosorbent Assay

    32) Product Images from "IL-17F Induces CCL20 in Bronchial Epithelial Cells"

    Article Title: IL-17F Induces CCL20 in Bronchial Epithelial Cells

    Journal: Journal of Allergy

    doi: 10.1155/2011/587204

    Effect of overexpression of dominant-negative mutants Raf1 and Ras on CCL20 protein expression in BEAS-2B cells. The cells overexpressing dominant-negative mutants were stimulated with IL-17F for 24 hrs, and CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P
    Figure Legend Snippet: Effect of overexpression of dominant-negative mutants Raf1 and Ras on CCL20 protein expression in BEAS-2B cells. The cells overexpressing dominant-negative mutants were stimulated with IL-17F for 24 hrs, and CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P

    Techniques Used: Over Expression, Dominant Negative Mutation, Expressing, Enzyme-linked Immunosorbent Assay

    Effect of MSK1 inhibitors, H89, and Ro318220 on IL-17F-induced CCL20. BEAS-2B cells were pretreated for 1 hr as indicated before the 24-hr stimulation of IL-17F, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P
    Figure Legend Snippet: Effect of MSK1 inhibitors, H89, and Ro318220 on IL-17F-induced CCL20. BEAS-2B cells were pretreated for 1 hr as indicated before the 24-hr stimulation of IL-17F, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P

    Techniques Used: Enzyme-linked Immunosorbent Assay

    Effect of siRNA for p90RSK, MSK1 and CREB on IL-17F-induced CCL20 expression. BEAS-2B cells transfected with siRNAs as indicated were stimulated with IL-17F for 24 hrs, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as mean s ± SEM ( n = 6). * P
    Figure Legend Snippet: Effect of siRNA for p90RSK, MSK1 and CREB on IL-17F-induced CCL20 expression. BEAS-2B cells transfected with siRNAs as indicated were stimulated with IL-17F for 24 hrs, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as mean s ± SEM ( n = 6). * P

    Techniques Used: Expressing, Transfection, Enzyme-linked Immunosorbent Assay

    The expression of CCL20 gene and protein by IL-17F in bronchial epithelial cells. (a) CCL20 gene expression by real-time PCR in BEAS-2B cells. Real-time PCR was performed as described in Materials and Methods. BEAS-2B cells were stimulated with IL-17F for 4 hrs ( n = 6). (c) CCL20 protein levels in supernatants in BEAS-2B cells. ELISA was performed ( n = 6). (d) CCL20 protein levels in supernatants in NHBEs ( n = 6). * P
    Figure Legend Snippet: The expression of CCL20 gene and protein by IL-17F in bronchial epithelial cells. (a) CCL20 gene expression by real-time PCR in BEAS-2B cells. Real-time PCR was performed as described in Materials and Methods. BEAS-2B cells were stimulated with IL-17F for 4 hrs ( n = 6). (c) CCL20 protein levels in supernatants in BEAS-2B cells. ELISA was performed ( n = 6). (d) CCL20 protein levels in supernatants in NHBEs ( n = 6). * P

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

    Effect of PD98059 (PD), U0126, Raf1 kinase inhibitor I (Raf I), SB202190 (SB), and SP600125 (SP) on CCL20 protein expression in BEAS-2Bs. The cells were pretreated for 1 hr as indicated before the 24-hr stimulation of IL-17F, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P
    Figure Legend Snippet: Effect of PD98059 (PD), U0126, Raf1 kinase inhibitor I (Raf I), SB202190 (SB), and SP600125 (SP) on CCL20 protein expression in BEAS-2Bs. The cells were pretreated for 1 hr as indicated before the 24-hr stimulation of IL-17F, and then CCL20 protein levels in supernatants were measured by ELISA. The values are expressed as means ± SEM ( n = 6). * P

    Techniques Used: Expressing, Enzyme-linked Immunosorbent Assay

    Related Articles

    other:

    Article Title: Antibody blockade of IL-17 family cytokines in immunity to acute murine oral mucosal candidiasis
    Article Snippet: Puel A., Döffinger R., Natividad A., Chrabieh M., Barcenas-Morales G., Picard C., Cobat A., Ouachée-Chardin M., Toulon A., Bustamante J., Al-Muhsen S., Al-Owain M., Arkwright P. D., Costigan C., McConnell V., Cant A. J., Abinun M., Polak M., Bougnères P. F., Kumararatne D., Marodi L., Nahum A., Roifman C., Blanche S., Fischer A., Bodemer C., Abel L., Lilic D., Casanova J. L. (2010) Autoantibodies against IL-17A, IL-17F, and IL-22 in patients with chronic mucocutaneous candidiasis and autoimmune polyendocrine syndrome type I. J. Exp.

    Enzyme-linked Immunosorbent Assay:

    Article Title: Inhibition of Rho-Kinase Downregulates Th17 Cells and Ameliorates Hepatic Fibrosis by Schistosoma japonicum Infection
    Article Snippet: Cytokine Assay Cytokines in the culture supernatants and sera were measured using ELISA as we previously reported [ , ]. .. IL-4 and IFN-γ were measured with OptEIA kits (BD Bioscience, San Jose, CA, USA); IL-17, IL-17F, and IL-21 were measured with DuoSet ELISA kits (R & D Systems, Minneapolis, MN, USA). .. ELISA plates were developed with 3,3′,5,5′-tetramethylbenzidine (TMB) substrate (BD Bioscience, San Jose, CA, USA) and read with a microplate reader.

    Article Title: Schizophyllum commune induces IL-17-mediated neutrophilic airway inflammation in OVA-induced asthma model mice
    Article Snippet: LDH activity in BAL fluid was measured using the LDH-Cytotoxic Test (Wako Chemicals). .. Cytokine levels in BAL fluid IFN-γ, IL-17A, IL-17F, IL-13, and IL-4 levels in BAL fluid were measured using enzyme-linked immunoassay (ELISA) kits (R & D Systems, Minnesota, USA), according to the manufacturer’s instructions. .. Lung histopathology Mouse lungs were fixed in 4% formaldehyde, routinely embedded in paraffin, and sectioned at a thickness of 4 µm.

    Blocking Assay:

    Article Title: Th17 cytokines differentiate obesity from obesity-associated type 2 diabetes and promote TNFα production
    Article Snippet: A cells were cultured at 1×106 cells/mL in “U” bottom wells in RPMI media supplemented with 10% FCS and antibiotics, and treated with α-CD3/α-CD28 for 40 hrs ( ). .. Blocking Antibody Studies Neutralizing antibodies specific to IL-17A (100 ng-1µg) and IL-17F (1 µg) (R & D Systems or LifeSpan BioSciences) or IgG isotype controls (0.1–20µg) were added at the same time as stimuli. .. Flow Cytometry Stimulated PBMCs were cultured with Brefeldin A (3µg/ml; eBioscience) added for the last 4hrs.

    Expressing:

    Article Title: IL-1?-INDUCED POST-TRANSITION EFFECT OF NF-KAPPAB PROVIDES TIME-DEPENDENT WAVE OF SIGNALS FOR INITIAL PHASE OF INTRAPOSTATIC INFLAMMATION
    Article Snippet: In some experiments mice were pretreated with dexamethasone (Dex) (10 mg/kg in PBS) by i.p. injection. .. The intraprostatic expression of chemokine receptors, adhesion molecules, surface cell markers, and interleukin in formalin-fixed paraffin-embedded prostate tissue was evaluated using the following markers: for chemokine receptors - CXCR1/IL-8RA (Santa Cruz Biotechnology, Santa Cruz, CA) and CXCR4 (R & D System, Minneapolis, MN); for adhesion molecules - VCAM1 (Santa Cruz); for neutrophils - NIMP-R14 (Santa Cruz); for mononuclear cells (MNC) - CD45 (R & D System); and for IL-17F - (R & D System). .. Immuno-histochemical staining for the markers mentioned above was performed using reagents and protocols from Biocare Medical (Concord, CA).

    Article Title: Heterogeneous expression pattern of interleukin 17A (IL-17A), IL-17F and their receptors in synovium of rheumatoid arthritis, psoriatic arthritis and osteoarthritis: possible explanation for nonresponse to anti-IL-17 therapy?
    Article Snippet: Synovial tissue biopsies were cut into 5-μm sections and mounted on StarFrost adhesive glass slides (Knittelgläser, Braunschweig, Germany), after which slides were sealed in parafilm (Bemis, Neenah, WI, USA) and stored at −80°C until further use. .. Antibodies To investigate the detailed expression pattern of IL-17 in synovium, tissue sections were stained using mouse monoclonal antibodies against IL-17A (immunoglobulin G1 (IgG1), clone 41802), IL-17F (IgG2a, clone 197315) and their receptors IL-17RA (IgG1, clone 133617) and IL-17RC (IgG2b, clone 309882), all from R & D Systems (Minneapolis, MN, USA). .. For colocalisation studies, we used antibodies against the transcription factor RORγt (RORc, mouse IgG2a; RayBiotech, Norcross, GA, USA), T cells (biotin-conjugated mouse anti-CD4: IgG1, clone RPA-T4; Biolegend, San Diego, CA, USA; and biotin-conjugated mouse anti-CD8: IgG1, clone RFT8; SouthernBiotech, Birmingham, AL), B cells (biotin-conjugated mouse anti-CD19; IgG1, clone HIB19; Biolegend), macrophages (biotin-conjugated mouse anti-CD68; IgG2b clone Y1/82A; Biolegend; and biotin-conjugated mouse anti-CD163; IgG1 clone GHI/61; Biolegend), neutrophils (biotin-conjugated mouse anti-CD15; IgM clone HI98; eBioscience, San Diego, CA, USA), mast cells (mouse anti–mast cell tryptase (MCT); IgG1 clone AA1; Dako, Glostrup, Denmark), lymphatic vessels (goat polyclonal anti-lymphatic vessel endothelial hyaluronan receptor 1 (Lyve-1); R & D Systems), blood vessels (mouse anti–von Willebrand factor (vWF); IgG1 clone F8/86; Dako) and high endothelial venules (mouse anti–peripheral lymph node addressin (PNAd); IgM clone MECA-79; Biolegend).

    Formalin-fixed Paraffin-Embedded:

    Article Title: IL-1?-INDUCED POST-TRANSITION EFFECT OF NF-KAPPAB PROVIDES TIME-DEPENDENT WAVE OF SIGNALS FOR INITIAL PHASE OF INTRAPOSTATIC INFLAMMATION
    Article Snippet: In some experiments mice were pretreated with dexamethasone (Dex) (10 mg/kg in PBS) by i.p. injection. .. The intraprostatic expression of chemokine receptors, adhesion molecules, surface cell markers, and interleukin in formalin-fixed paraffin-embedded prostate tissue was evaluated using the following markers: for chemokine receptors - CXCR1/IL-8RA (Santa Cruz Biotechnology, Santa Cruz, CA) and CXCR4 (R & D System, Minneapolis, MN); for adhesion molecules - VCAM1 (Santa Cruz); for neutrophils - NIMP-R14 (Santa Cruz); for mononuclear cells (MNC) - CD45 (R & D System); and for IL-17F - (R & D System). .. Immuno-histochemical staining for the markers mentioned above was performed using reagents and protocols from Biocare Medical (Concord, CA).

    Staining:

    Article Title: Heterogeneous expression pattern of interleukin 17A (IL-17A), IL-17F and their receptors in synovium of rheumatoid arthritis, psoriatic arthritis and osteoarthritis: possible explanation for nonresponse to anti-IL-17 therapy?
    Article Snippet: Synovial tissue biopsies were cut into 5-μm sections and mounted on StarFrost adhesive glass slides (Knittelgläser, Braunschweig, Germany), after which slides were sealed in parafilm (Bemis, Neenah, WI, USA) and stored at −80°C until further use. .. Antibodies To investigate the detailed expression pattern of IL-17 in synovium, tissue sections were stained using mouse monoclonal antibodies against IL-17A (immunoglobulin G1 (IgG1), clone 41802), IL-17F (IgG2a, clone 197315) and their receptors IL-17RA (IgG1, clone 133617) and IL-17RC (IgG2b, clone 309882), all from R & D Systems (Minneapolis, MN, USA). .. For colocalisation studies, we used antibodies against the transcription factor RORγt (RORc, mouse IgG2a; RayBiotech, Norcross, GA, USA), T cells (biotin-conjugated mouse anti-CD4: IgG1, clone RPA-T4; Biolegend, San Diego, CA, USA; and biotin-conjugated mouse anti-CD8: IgG1, clone RFT8; SouthernBiotech, Birmingham, AL), B cells (biotin-conjugated mouse anti-CD19; IgG1, clone HIB19; Biolegend), macrophages (biotin-conjugated mouse anti-CD68; IgG2b clone Y1/82A; Biolegend; and biotin-conjugated mouse anti-CD163; IgG1 clone GHI/61; Biolegend), neutrophils (biotin-conjugated mouse anti-CD15; IgM clone HI98; eBioscience, San Diego, CA, USA), mast cells (mouse anti–mast cell tryptase (MCT); IgG1 clone AA1; Dako, Glostrup, Denmark), lymphatic vessels (goat polyclonal anti-lymphatic vessel endothelial hyaluronan receptor 1 (Lyve-1); R & D Systems), blood vessels (mouse anti–von Willebrand factor (vWF); IgG1 clone F8/86; Dako) and high endothelial venules (mouse anti–peripheral lymph node addressin (PNAd); IgM clone MECA-79; Biolegend).

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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
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    R&D Systems il 17a
    Neutrophils are reduced in the joints of Il17ra −/− mice and are unresponsive to direct stimulation with <t>IL-17A.</t> A, Number of neutrophils in the ankle joints of WT and Il17ra −/− mice on day 12 was determined by FACS analysis counting Ly6G + cells in relation to counting beads. Data are presented as mean ± SEM (n = 3 mice per group). One of three independent experiments is shown. B, Chemotaxis of freshly isolated murine bone marrow-derived neutrophils towards 100 nM LTB 4 and IL-17A (10 and 100 ng/ml) assessed using 24-well transwell assays. Data represent numbers of migrated neutrophils (n = 3 independently performed experiments). C, Chemotaxis of freshly isolated murine bone marrow-derived neutrophils towards LTB 4 (100 nM) MIP-2 (100 nM) and IL-17A (1, 10, 100, 1000 ng/ml) as well as their corresponding chemokinesis controls assessed using 96-well ChemoTx assays. Data are presented as chemotactic index (number of cells migrating to chemoattractant/number of cell migrating to medium control). Data shown are mean ± SEM (n = 4 independently performed experiments). D, Levels of IL-17RA and IL-17RC mRNA determined by qPCR on RNA isolated from murine FLS and freshly isolated bone marrow-derived neutrophils (n = 3 independently performed experiments). Data were compared by unpaired two-tailed Student's t test, ** = p
    Il 17a, supplied by R&D Systems, 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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    R&D Systems goat anti mouse il 17
    Tbet deficiency prevents induction of transplantation tolerance by combined co-stimulation blockade with persistent T17/Th2 skewing of alloantigen specific cytokine profile, and PMN, CD4, and <t>IL-17-producing</t> CD8 T cell infiltration. ( A ) Kaplan-Meier survival
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    R&D Systems il 17f
    Immunostaining for chemoattractant receptor CXCR1/IL-8RA and <t>IL-17F</t> in representative samples of prostates from C57BL/6J mice. IL-1 β (10 μg/kg) was i.v. injected in the tail vein. To proof pro-inflammatory ability of IL-1 β along
    Il 17f, 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
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    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

    Neutrophils are reduced in the joints of Il17ra −/− mice and are unresponsive to direct stimulation with IL-17A. A, Number of neutrophils in the ankle joints of WT and Il17ra −/− mice on day 12 was determined by FACS analysis counting Ly6G + cells in relation to counting beads. Data are presented as mean ± SEM (n = 3 mice per group). One of three independent experiments is shown. B, Chemotaxis of freshly isolated murine bone marrow-derived neutrophils towards 100 nM LTB 4 and IL-17A (10 and 100 ng/ml) assessed using 24-well transwell assays. Data represent numbers of migrated neutrophils (n = 3 independently performed experiments). C, Chemotaxis of freshly isolated murine bone marrow-derived neutrophils towards LTB 4 (100 nM) MIP-2 (100 nM) and IL-17A (1, 10, 100, 1000 ng/ml) as well as their corresponding chemokinesis controls assessed using 96-well ChemoTx assays. Data are presented as chemotactic index (number of cells migrating to chemoattractant/number of cell migrating to medium control). Data shown are mean ± SEM (n = 4 independently performed experiments). D, Levels of IL-17RA and IL-17RC mRNA determined by qPCR on RNA isolated from murine FLS and freshly isolated bone marrow-derived neutrophils (n = 3 independently performed experiments). Data were compared by unpaired two-tailed Student's t test, ** = p

    Journal: PLoS ONE

    Article Title: IL-17RA Signaling Amplifies Antibody-Induced Arthritis

    doi: 10.1371/journal.pone.0026342

    Figure Lengend Snippet: Neutrophils are reduced in the joints of Il17ra −/− mice and are unresponsive to direct stimulation with IL-17A. A, Number of neutrophils in the ankle joints of WT and Il17ra −/− mice on day 12 was determined by FACS analysis counting Ly6G + cells in relation to counting beads. Data are presented as mean ± SEM (n = 3 mice per group). One of three independent experiments is shown. B, Chemotaxis of freshly isolated murine bone marrow-derived neutrophils towards 100 nM LTB 4 and IL-17A (10 and 100 ng/ml) assessed using 24-well transwell assays. Data represent numbers of migrated neutrophils (n = 3 independently performed experiments). C, Chemotaxis of freshly isolated murine bone marrow-derived neutrophils towards LTB 4 (100 nM) MIP-2 (100 nM) and IL-17A (1, 10, 100, 1000 ng/ml) as well as their corresponding chemokinesis controls assessed using 96-well ChemoTx assays. Data are presented as chemotactic index (number of cells migrating to chemoattractant/number of cell migrating to medium control). Data shown are mean ± SEM (n = 4 independently performed experiments). D, Levels of IL-17RA and IL-17RC mRNA determined by qPCR on RNA isolated from murine FLS and freshly isolated bone marrow-derived neutrophils (n = 3 independently performed experiments). Data were compared by unpaired two-tailed Student's t test, ** = p

    Article Snippet: In order to determine which of the genes downregulated in the ankles of Il17ra−/− mice might be directly regulated by IL-17RA signaling, murine fibroblast-like synoviocytes (FLS) were either left unstimulated or stimulated with 100 ng/ml IL-17A for 16 h. RNA was then isolated and gene expression assessed by qPCR.

    Techniques: Mouse Assay, FACS, Chemotaxis Assay, Isolation, Derivative Assay, Real-time Polymerase Chain Reaction, Two Tailed Test

    Tbet deficiency prevents induction of transplantation tolerance by combined co-stimulation blockade with persistent T17/Th2 skewing of alloantigen specific cytokine profile, and PMN, CD4, and IL-17-producing CD8 T cell infiltration. ( A ) Kaplan-Meier survival

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

    Article Title: Targeting Tim-1 to overcome resistance to transplantation tolerance mediated by CD8 T17 cells

    doi: 10.1073/pnas.0812538106

    Figure Lengend Snippet: Tbet deficiency prevents induction of transplantation tolerance by combined co-stimulation blockade with persistent T17/Th2 skewing of alloantigen specific cytokine profile, and PMN, CD4, and IL-17-producing CD8 T cell infiltration. ( A ) Kaplan-Meier survival

    Article Snippet: Frozen sections were used for immunofluorescence staining using goat anti-mouse IL-17 (R & D Systems), rat anti-Mouse CD4 and CD8 (both from BioExpress) as primary antibodies.

    Techniques: Transplantation Assay

    In vivo IL-17 neutralization inhibits rejection and facilitates allograft survival with combined co-stimulation blockade in Tbet KO recipients. ( A ) Fully mismatched cardiac allograft survival in Tbet KO recipients treated with CTLA4Ig+MR1 and anti-IL-17

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

    Article Title: Targeting Tim-1 to overcome resistance to transplantation tolerance mediated by CD8 T17 cells

    doi: 10.1073/pnas.0812538106

    Figure Lengend Snippet: In vivo IL-17 neutralization inhibits rejection and facilitates allograft survival with combined co-stimulation blockade in Tbet KO recipients. ( A ) Fully mismatched cardiac allograft survival in Tbet KO recipients treated with CTLA4Ig+MR1 and anti-IL-17

    Article Snippet: Frozen sections were used for immunofluorescence staining using goat anti-mouse IL-17 (R & D Systems), rat anti-Mouse CD4 and CD8 (both from BioExpress) as primary antibodies.

    Techniques: In Vivo, Neutralization

    Immunostaining for chemoattractant receptor CXCR1/IL-8RA and IL-17F in representative samples of prostates from C57BL/6J mice. IL-1 β (10 μg/kg) was i.v. injected in the tail vein. To proof pro-inflammatory ability of IL-1 β along

    Journal:

    Article Title: IL-1?-INDUCED POST-TRANSITION EFFECT OF NF-KAPPAB PROVIDES TIME-DEPENDENT WAVE OF SIGNALS FOR INITIAL PHASE OF INTRAPOSTATIC INFLAMMATION

    doi: 10.1002/pros.20916

    Figure Lengend Snippet: Immunostaining for chemoattractant receptor CXCR1/IL-8RA and IL-17F in representative samples of prostates from C57BL/6J mice. IL-1 β (10 μg/kg) was i.v. injected in the tail vein. To proof pro-inflammatory ability of IL-1 β along

    Article Snippet: The intraprostatic expression of chemokine receptors, adhesion molecules, surface cell markers, and interleukin in formalin-fixed paraffin-embedded prostate tissue was evaluated using the following markers: for chemokine receptors - CXCR1/IL-8RA (Santa Cruz Biotechnology, Santa Cruz, CA) and CXCR4 (R & D System, Minneapolis, MN); for adhesion molecules - VCAM1 (Santa Cruz); for neutrophils - NIMP-R14 (Santa Cruz); for mononuclear cells (MNC) - CD45 (R & D System); and for IL-17F - (R & D System).

    Techniques: Immunostaining, Mouse Assay, Injection

    Systemic administration of IL-1β induces multitype time-dependent behavior of intraprostatic chemoattractant receptors and IL-17F

    Journal:

    Article Title: IL-1?-INDUCED POST-TRANSITION EFFECT OF NF-KAPPAB PROVIDES TIME-DEPENDENT WAVE OF SIGNALS FOR INITIAL PHASE OF INTRAPOSTATIC INFLAMMATION

    doi: 10.1002/pros.20916

    Figure Lengend Snippet: Systemic administration of IL-1β induces multitype time-dependent behavior of intraprostatic chemoattractant receptors and IL-17F

    Article Snippet: The intraprostatic expression of chemokine receptors, adhesion molecules, surface cell markers, and interleukin in formalin-fixed paraffin-embedded prostate tissue was evaluated using the following markers: for chemokine receptors - CXCR1/IL-8RA (Santa Cruz Biotechnology, Santa Cruz, CA) and CXCR4 (R & D System, Minneapolis, MN); for adhesion molecules - VCAM1 (Santa Cruz); for neutrophils - NIMP-R14 (Santa Cruz); for mononuclear cells (MNC) - CD45 (R & D System); and for IL-17F - (R & D System).

    Techniques: