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easygo! mouse il-17a one-step elisa kit  (Multi Sciences (Lianke) Biotech Co Ltd)


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    Multi Sciences (Lianke) Biotech Co Ltd easygo! mouse il-17a one-step elisa kit
    Easygo! Mouse Il 17a One Step Elisa Kit, supplied by Multi Sciences (Lianke) Biotech Co Ltd, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/il+17a+elisa+kit/EasyGo!+Mouse+IL-17A+One-Step+ELISA+Kit/custom%40ek217eg%4042484797
    Average 93 stars, based on 1 article reviews
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    Related Articles

    Cell Culture:

    Article Title: Circular RNA circPHF16 enhances IL-17A expression and secretion by sequestering miR-378a-3p to activate the IL6ST axis in Graves' disease.
    Article Snippet: Interleukin-17A (IL-17A) plays a pivotal role in the pathogenesis of Graves’ disease (GD), an autoimmune disorder affecting thyroid function, but the detailed regulatory mechanisms remain elusive.. Circular RNAs (circRNAs) have emerged as key regulators of IL-17A expression and secretion in autoimmune diseases, yet their specific role in GD, especially within CD4 + T lymphocytes, are not well understood.. In this study, a circRNA, circPHF16 (hsa_circ_0090364) was found to be highly expressed in the peripheral blood mononuclear cells and serum of GD patients.

    Enzyme-linked Immunosorbent Assay:

    Article Title: Circular RNA circPHF16 enhances IL-17A expression and secretion by sequestering miR-378a-3p to activate the IL6ST axis in Graves' disease.
    Article Snippet: Interleukin-17A (IL-17A) plays a pivotal role in the pathogenesis of Graves’ disease (GD), an autoimmune disorder affecting thyroid function, but the detailed regulatory mechanisms remain elusive.. Circular RNAs (circRNAs) have emerged as key regulators of IL-17A expression and secretion in autoimmune diseases, yet their specific role in GD, especially within CD4 + T lymphocytes, are not well understood.. In this study, a circRNA, circPHF16 (hsa_circ_0090364) was found to be highly expressed in the peripheral blood mononuclear cells and serum of GD patients.

    Article Title: Triptolide alleviates rheumatoid arthritis by inhibiting lactate-mediated activation of mTORC1/HIF-1α to restrain Th17 cell differentiation.
    Article Snippet: Background: Triptolide (TP), a diterpenoid isolated from Tripterygium wilfordii Hook. f. (TWHF), has potent antiinflammatory and immunomodulatory activities and has shown therapeutic efficacy in various autoimmune diseases.. However, the mechanism by which TP alleviates rheumatoid arthritis (RA) remains unclear.. Methods: Using a collagen-induced arthritis (CIA) mouse model and an in vitro Th17 differentiation model, we investigated the effects of TP on RA symptoms by examining its regulation of Th17 cell differentiation from the perspective of lactate metabolism.

    Lactate Assay:

    Article Title: Triptolide alleviates rheumatoid arthritis by inhibiting lactate-mediated activation of mTORC1/HIF-1α to restrain Th17 cell differentiation.
    Article Snippet: Background: Triptolide (TP), a diterpenoid isolated from Tripterygium wilfordii Hook. f. (TWHF), has potent antiinflammatory and immunomodulatory activities and has shown therapeutic efficacy in various autoimmune diseases.. However, the mechanism by which TP alleviates rheumatoid arthritis (RA) remains unclear.. Methods: Using a collagen-induced arthritis (CIA) mouse model and an in vitro Th17 differentiation model, we investigated the effects of TP on RA symptoms by examining its regulation of Th17 cell differentiation from the perspective of lactate metabolism.



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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 <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 <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 <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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    Image Search Results


    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: