il 17a elisa kits (Elabscience Biotechnology)
Elabscience Biotechnology is a verified supplier 
Elabscience Biotechnology manufactures this product 
95
Structured Review
Elabscience Biotechnology
il 17a elisa kits
Il 17a Elisa Kits, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 63 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse+il+17a+elisa+kit/Mouse%3FIL-17A+(Interleukin%3F17A)%3FELISA%3FKit/pmc13673060-218-9-12
Average 95 stars, based on 63 article reviews
Il 17a Elisa Kits, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 63 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse+il+17a+elisa+kit/Mouse%3FIL-17A+(Interleukin%3F17A)%3FELISA%3FKit/pmc13673060-218-9-12
Average 95 stars, based on 63 article reviews
il 17a elisa kits - by Bioz Stars,
2026-11
95/100 stars
Images
1) Product Images from "Gut Microbiota‐Derived Indole‐3‐Acetaldehyde Contributes to the Disease‐Alleviating Effects of Kurarinone in Experimental Autoimmune Encephalomyelitis"
Article Title: Gut Microbiota‐Derived Indole‐3‐Acetaldehyde Contributes to the Disease‐Alleviating Effects of Kurarinone in Experimental Autoimmune Encephalomyelitis
Journal: Advanced Science
doi: 10.1002/advs.78358
Figure Legend Snippet: KU treatment mitigates EAE and reduces Th1 and Th17 cell proportions in mice. (A) Schematic timeline of EAE induction and KU administration (100 mg kg −1 , intragastric). Mice were immunized with MOG 35‐55 peptide, and KU or vehicle was administered from 11 to 21 dpi. (B) Line graph of clinical scores in the control (Ctrl), vehicle‐treated EAE, and KU‐treated EAE groups ( n = 8 per group). (C) Disease incidence curves of EAE mice. (D) Cumulative clinical scores and peak score in each group. (E) Representative HE staining and LFB staining of spinal cord from the Ctrl, vehicle‐treated EAE, and KU‐treated EAE groups. (F) Inflammation and demyelination scores based on HE and LFB staining ( n = 6 per group). (G) The proportion of CD3 + CD4 + T cells in the CNS and spleen (SP) ( n = 3–4 per group). (H) Absolute counts of CD3 + and CD4 + T cells in the CNS of each group. (I) The proportion of CD4 + IFNγ + (Th1) cells in the CNS and SP. (J) The proportion of CD4 + IL‐17A + (Th17) cells in the CNS and SP. (K) Relative mRNA expression of T‐bet and RORγt in the spinal cord measured by qPCR. (L) ELISA detection of serum IFNγ and IL‐17A concentrations in each group. Data are presented as mean ± SEM; * p < 0.05, ** p < 0.01, *** p < 0.001 vs. vehicle‐treated EAE.
Techniques Used: Control, H&E Stain, Staining, Expressing, Enzyme-linked Immunosorbent Assay
Figure Legend Snippet: KU modulates gut microbiota to ameliorate EAE. (A) Alpha diversity (Shannon index) of gut microbiota in the Ctrl, vehicle‐treated EAE, and KU‐treated EAE groups ( n = 8 per group). Pair‐wise comparisons were performed using Wilcoxon rank‐sum test. (B) Principal coordinate analysis (PCoA) of gut microbiota based on Bray‐Curtis distance (pseudo‐ F = 30.12, R 2 = 0.741, p < 0.001); each dot represents an individual sample. (C) Stacked bar plot showing the relative abundance of gut microbiota at the family level in the Ctrl, vehicle‐treated EAE, and KU‐treated EAE groups. (D) Schematic timeline of ABX treatment and FMT and EAE induction: EAE mice received FMT from vehicle‐treated or KU‐treated donor mice (100 mg kg −1 , intragastric). (E) Clinical scores of FMT‐Vehicle and FMT‐KU groups ( n = 9 per group). (F) Disease incidence curves of EAE mice. (G) Statistical analysis of cumulative clinical scores and peak score. (H) Representative HE staining and LFB staining of spinal cord tissues from FMT‐Vehicle and FMT‐KU mice. (I) Inflammation score and demyelination score in the spinal cord ( n = 4 per group). (J) Flow cytometric plots of CD4 + IFNγ + (Th1) and CD4 + IL‐17A + (Th17) cells in the CNS and SP. (K) Quantification of CD4 + IFNγ + and CD4 + IL‐17A + cell percentages in the CNS and SP ( n = 5 per group). Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. EAE mice that received FMT from vehicle‐treated donors.
Techniques Used: Analysis, H&E Stain, Staining
Figure Legend Snippet: KU ameliorates EAE in an A. muciniphila ‐dependent manner. (A) Heatmap showing the relative abundance of the top 10 gut microbial species in the Ctrl, vehicle‐treated EAE, and KU‐treated groups ( n = 8 per group). (B) Linear discriminant analysis effect size (LEfSe) analysis was performed to screen differentially abundant microbial taxa across the three groups. Taxa with an LDA score > 3 were defined as potential microbial biomarkers with statistical significance. (C) Schematic timeline of ABX pretreatment, KU administration, A. muciniphila supplementation, and EAE induction. (D) Clinical scores of EAE, EAE+ABX, EAE+ABX+KU, and EAE+ABX+KU+ A. muciniphila ( n = 8 per group). (E) Cumulative clinical scores and peak score in each group. (F) Representative HE staining and LFB staining of the spinal cord. (G) Spinal cord inflammation score and demyelination score ( n = 4 per group). (H) Flow cytometric plots of CD4 + IFNγ + (Th1) cells in the CNS and SP of each group. (I) Quantification of CD4 + IFNγ + cell percentages in the CNS and SP ( n = 4 per group). (J) Flow cytometric plots of CD4 + IL‐17A + (Th17) cells in the CNS and SP of each group. (K) Quantification of CD4 + IL‐17A + cell percentages in the CNS and SP ( n = 4 per group). Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001; ns, p > 0.05.
Techniques Used: Analysis, H&E Stain, Staining
Figure Legend Snippet: IAAld alleviates EAE and reduces Th1 and Th17 cell proportions. (A) Schematic timeline of EAE induction and IAAld administration ( n = 8 per group). (B) Clinical scores of vehicle‐treated EAE, EAE+IAAld 40 mg/kg/day (IAAld 40), and EAE+IAAld 80 mg/kg/day (IAAld 80) groups. (C) Disease incidence curves of EAE mice with different doses of IAAld treatment. (D) Quantification of cumulative clinical scores and peak score in each group. (E) Representative HE staining and LFB staining of spinal cord tissues from the vehicle‐treated EAE, IAAld 40, and IAAld 80 groups. (F) Spinal cord inflammation score and demyelination score ( n = 3 per group). (G) Flow cytometric plots of CD4 + IFNγ + (Th1) and CD4 + IL‐17A + (Th17) cells in the CNS and SP of each group. (H) Quantification of CD4 + IFNγ + and CD4 + IL‐17A + cell percentages in the CNS and SP ( n = 4 per group). Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.
Techniques Used: H&E Stain, Staining
Figure Legend Snippet: IAAld suppresses Th1 and Th17 cell differentiation in an AhR‐dependent manner by repressing JAK/STAT signaling. (A) KEGG pathway enrichment analysis of the intersectional targets of IAAld and MS. (B) In silico prediction of the binding interaction between IAAld and AhR by molecular docking. The calculated binding energy (BE) is −6.6 kcal/mol (inset: chemical structure of IAAld). (C,D) Flow cytometric quantification and representative plots of CD4 + IFNγ + (Th1) and CD4 + IL‑17A + (Th17) cells under in vitro differentiation conditions across PBS, IAAld (10 µM), and IAAld+siAhR (AhR knockdown by siRNA) groups ( n = 3 per group). (E) Immunofluorescence staining of AhR (green) in Th1 and Th17 cells of each group, and cell nuclei were stained with DAPI (blue). (F) Western blot analysis showing protein levels of AhR, p‑JAK2, JAK2, p‑STAT4, STAT4, p‑STAT3, STAT3, SOCS1, SOCS3, and GAPDH in Th1 (left) and Th17 (right) cells. (G) Quantitative analysis of AhR/GAPDH ratio, p‐JAK2/JAK2 ratio, p‐STAT4/STAT4 ratio, p‐STAT3/STAT3 ratio, SOCS1/GAPDH ratio and SOCS3/GAPDH ratio in each group ( n = 4 per group). Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.
Techniques Used: Cell Differentiation, Analysis, In Silico, Binding Assay, Docking Assay, In Vitro, Knockdown, Immunofluorescence, Staining, Western Blot, Significance Assay
Figure Legend Snippet: IAAld treatment mitigates EAE in an AhR‐dependent manner. (A) Relative mRNA expression levels of Ahr, Cyp1a1, and Cyp1b1 in the spinal cord of EAE mice treated with vehicle, IAAld 40, or IAAld 80 groups. (B) Schematic timeline depicting the experimental protocol for EAE induction, followed by administration of IAAld (80 mg/kg/day) and AhR inhibitor (AhRi; SR1, 50 mg/kg/day). (C) Clinical scores for EAE mice treated with vehicle, IAAld, and IAAld+AhRi groups ( n = 6 per group). (D) Disease incidence curves for EAE mice over time. (E) Quantification of cumulative clinical scores and peak score for each group. (F) Representative HE and LFB staining of spinal cord tissues for assessment of inflammation and demyelination, respectively. (G) Quantification of spinal cord inflammation and demyelination scores ( n = 3 per group). (H) Representative flow cytometry plots indicating the percentages of CD4 + IFNγ + (Th1) and CD4 + IL‐17A + (Th17) cells in the CNS and SP of each group. (I) Quantification of CD4 + IFNγ + and CD4 + IL‐17A + cell percentages in the CNS and SP across groups ( n = 3–4 per group). Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.
Techniques Used: Expressing, Staining, Flow Cytometry
Related Articles
Enzyme-linked Immunosorbent Assay:Article Title: Effects of topical isoxsuprine ointment on imiquimod-induced psoriasiform skin inflammation in mice. Article Snippet: This study assesses the potential positive impact of a 0.05% isoxsuprine ointment on psoriasiform skin inflammation generated by imiquimod in mouse models.. Thirty-two male albino mice were allocated into four groups: the control group (which received topical emollients twice daily for 16 days), the induction group (which received imiquimod cream (5%) for 8 days, twice daily followed by petrolatum gel (15%) for another 8 days), and the other two groups, which received imiquimod cream (5%) for 8 days followed by either clobetasol ointment (0.05%) or isoxsuprine ointment (0.05%) twice daily for an additional 8 days.. At the end of the experiment, mice were sacrificed by ethical standards, and levels of TNF-α, IL-6, IL17A, IL-23, and VEGF were measured; PASI and Backer’s score were examined, in addition to the histopathology of skin tissue. Article Title: Cordycepin Mitigates Sepsis-Associated Encephalopathy by Promoting Microglial M2 Polarization via the IL-17a/IL-17RA/NF-κB Axis. Article Snippet: Sepsis-associated encephalopathy (SAE) is a serious neurological complication of systemic infection, marked by cognitive deficits, neuroinflammation, and increased mortality.. Microglial activation and proinflammatory signaling pathways, particularly involving IL-17a and NF-κB, are key contributors to SAE pathogenesis.. Cordycepin (3′-deoxyadenosine), a bioactive nucleoside analog from Cordyceps militaris, exhibits potent anti-inflammatory and immunomodulatory effects, yet its role in SAE remains largely unexplored. Article Title: MMP12 exacerbates pulmonary inflammation by enhancing IL-17A expression Article Snippet: .. The Human IL-17A ELISA Kit (Cat#E-EL-H5812), Human TNF-α ELISA Kit (Cat#E-EL-H0109), Human S100A9 ELISA Kit (Cat#E-EL-H6197), Human MMP12 ELISA Kit (Cat#E-EL-H0133), and Article Title: Activation of IL-17/CEBPB/PFKFB3 triggers energy metabolic switching and goblet cell differentiation in ulcerative colitis. Article Snippet: This is a PDF of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability.. This version will undergo additional copyediting, typesetting and review before it is published in its final form.. As such, this version is no longer the Accepted Manuscript, but it is not yet the definitive Version of Record; we are providing this early version to give early visibility of the article. Article Title: Abnormal purine metabolism in nasal epithelial cells affects allergic rhinitis by regulating Th17/Treg cells. Article Snippet: We aimed to explore novel pathogenesis in young children with allergic rhinitis (AR), and thus finding novel nasal spray reagents for them, especially under 4 yr old.. In this study, nontargeted metabolomics analyses were used to explore the differential metabolites in nasal lavage fluid (NALF) of children with AR.. Cell Counting Kit-8 (CCK-8) and flow cytometry were used to assess cell proliferation and apoptosis in human nasal mucosal epithelial cells (HNEpCs). |
