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apc anti human il 17a  (MedChemExpress)


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    Structured Review

    MedChemExpress apc anti human il 17a
    Apc Anti Human Il 17a, supplied by MedChemExpress, 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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    Club cell AHR is required for EPFR-induced pulmonary Th17 responses and neutrophilic inflammation. (a) Schematic of the experimental design: tamoxifen was administered for 5 consecutive days to induce Cre recombinase-mediated deletion of Ahr in club cells, followed by a 7-day washout period. Male and female Cre-negative Ahr fl/fl LM or Ahr ΔCC mice were then exposed to air or EPFRs by inhalation from day 0 through day 6. Lungs and bronchoalveolar lavage fluid (BALF) were collected on day 6 post-exposure. (b) Flow cytometric quantification of Th17 cells i.e. IL-17 producing CD4 + T cells (Lin − CD45 + CD3 + CD4 + ) in lungs of air or EPFR-exposed LM and Ahr ΔCC mice; n = 6 to 10 mice per group. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05) (c) Concatenated pseudo color dot plots of CD4 + T cells gated <t>for</t> <t>IL-17A</t> in air or EPFR-exposed LM and Ahr ΔCC mice; n = 6 to 10 mice. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05) (d) Total and differential BALF cell counts from air or EPFR-exposed LM and Ahr ΔCC mice; n = 4 to 6 mice per group. Data are presented as mean ± SEM. Statistical significance was determined using one-way ANOVA followed by Tukey's post-hoc test; a p <0.05 compared to Air-LM and b p < 0.05 compared to EPFR-LM. (e) Representative BALF cell images from LM and Ahr ΔCC mice exposed to air or EPFR; arrows indicate neutrophils. Scale bar = 25 μm. (f-j) Analysis of BALF pro-inflammatory cytokines (IL-17, KC/GRO, IL-6, IL-1β, TNF-α) from air or EPFR-exposed LM and Ahr ΔCC mice; n = 4 to 7 mice per group. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05).
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    Club cell AHR is required for EPFR-induced pulmonary Th17 responses and neutrophilic inflammation. (a) Schematic of the experimental design: tamoxifen was administered for 5 consecutive days to induce Cre recombinase-mediated deletion of Ahr in club cells, followed by a 7-day washout period. Male and female Cre-negative Ahr fl/fl LM or Ahr ΔCC mice were then exposed to air or EPFRs by inhalation from day 0 through day 6. Lungs and bronchoalveolar lavage fluid (BALF) were collected on day 6 post-exposure. (b) Flow cytometric quantification of Th17 cells i.e. IL-17 producing CD4 + T cells (Lin − CD45 + CD3 + CD4 + ) in lungs of air or EPFR-exposed LM and Ahr ΔCC mice; n = 6 to 10 mice per group. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05) (c) Concatenated pseudo color dot plots of CD4 + T cells gated for IL-17A in air or EPFR-exposed LM and Ahr ΔCC mice; n = 6 to 10 mice. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05) (d) Total and differential BALF cell counts from air or EPFR-exposed LM and Ahr ΔCC mice; n = 4 to 6 mice per group. Data are presented as mean ± SEM. Statistical significance was determined using one-way ANOVA followed by Tukey's post-hoc test; a p <0.05 compared to Air-LM and b p < 0.05 compared to EPFR-LM. (e) Representative BALF cell images from LM and Ahr ΔCC mice exposed to air or EPFR; arrows indicate neutrophils. Scale bar = 25 μm. (f-j) Analysis of BALF pro-inflammatory cytokines (IL-17, KC/GRO, IL-6, IL-1β, TNF-α) from air or EPFR-exposed LM and Ahr ΔCC mice; n = 4 to 7 mice per group. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05).

    Journal: Redox Biology

    Article Title: Aryl hydrocarbon receptor in club cells drives Th17-mediated lung injury following inhalation exposure to environmentally persistent free radicals

    doi: 10.1016/j.redox.2026.104105

    Figure Lengend Snippet: Club cell AHR is required for EPFR-induced pulmonary Th17 responses and neutrophilic inflammation. (a) Schematic of the experimental design: tamoxifen was administered for 5 consecutive days to induce Cre recombinase-mediated deletion of Ahr in club cells, followed by a 7-day washout period. Male and female Cre-negative Ahr fl/fl LM or Ahr ΔCC mice were then exposed to air or EPFRs by inhalation from day 0 through day 6. Lungs and bronchoalveolar lavage fluid (BALF) were collected on day 6 post-exposure. (b) Flow cytometric quantification of Th17 cells i.e. IL-17 producing CD4 + T cells (Lin − CD45 + CD3 + CD4 + ) in lungs of air or EPFR-exposed LM and Ahr ΔCC mice; n = 6 to 10 mice per group. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05) (c) Concatenated pseudo color dot plots of CD4 + T cells gated for IL-17A in air or EPFR-exposed LM and Ahr ΔCC mice; n = 6 to 10 mice. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05) (d) Total and differential BALF cell counts from air or EPFR-exposed LM and Ahr ΔCC mice; n = 4 to 6 mice per group. Data are presented as mean ± SEM. Statistical significance was determined using one-way ANOVA followed by Tukey's post-hoc test; a p <0.05 compared to Air-LM and b p < 0.05 compared to EPFR-LM. (e) Representative BALF cell images from LM and Ahr ΔCC mice exposed to air or EPFR; arrows indicate neutrophils. Scale bar = 25 μm. (f-j) Analysis of BALF pro-inflammatory cytokines (IL-17, KC/GRO, IL-6, IL-1β, TNF-α) from air or EPFR-exposed LM and Ahr ΔCC mice; n = 4 to 7 mice per group. Data are presented as mean ± SEM and normalized to air controls of the respective genotype. Statistical significance was determined using Student's t-test (∗p < 0.05).

    Article Snippet: IL-17A levels in BALF samples were measured using a commercially available Mouse IL-17A Sandwich ELISA Kit (Proteintech, Rosemont, IL; catalog# KE10020) according to the manufacturer's instructions.

    Techniques:

    Overview of the immunopathogenesis and therapeutic targets of psoriasis. Epidermal damage triggers innate immune activation, promoting dendritic cell-mediated production of IL-23 and IL-12, which induce Th17- and Th1-dependent inflammatory responses, respectively. IL-17A and IL-17F subsequently act on keratinocytes via the IL-17 receptor complex, leading to keratinocyte activation and epidermal hyperplasia. Current injectable biologics (blue) and non-injectable small molecules or peptide inhibitors (red) targeting the IL-23/IL-17 axis are illustrated. pDC, plasmacytoid dendritic cell; mDC, myeloid dendritic cell.

    Journal: Biomolecules & Therapeutics

    Article Title: Current and Emerging Therapies Targeting the IL-23/IL-17 Axis in Psoriasis

    doi: 10.4062/biomolther.2026.019

    Figure Lengend Snippet: Overview of the immunopathogenesis and therapeutic targets of psoriasis. Epidermal damage triggers innate immune activation, promoting dendritic cell-mediated production of IL-23 and IL-12, which induce Th17- and Th1-dependent inflammatory responses, respectively. IL-17A and IL-17F subsequently act on keratinocytes via the IL-17 receptor complex, leading to keratinocyte activation and epidermal hyperplasia. Current injectable biologics (blue) and non-injectable small molecules or peptide inhibitors (red) targeting the IL-23/IL-17 axis are illustrated. pDC, plasmacytoid dendritic cell; mDC, myeloid dendritic cell.

    Article Snippet: , Izokibep/ABY-035 , IL-17A affibody , PsO, PsA , SC , , Phase 2 completed/ NCT03591887 (PsO) Phase 2b/3 terminated/ NCT05623345 (PsA).

    Techniques: Biomarker Discovery, Activation Assay