Human IL-17A (homodimer) ELISA kit
- Known as:
- Human Interleukin-17A (homodimer) Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- WHI019
- Product Quantity:
- 96T
- Category:
- -
- Supplier:
- Meretciel
- Gene target:
- Human IL-17A (homodimer) ELISA kit
Related genes to: Human IL-17A (homodimer) ELISA kit
- Gene:
- IL17A NIH gene
- Name:
- interleukin 17A
- Previous symbol:
- CTLA8, IL17
- Synonyms:
- IL-17A, IL-17
- Chromosome:
- 6p12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-10-25
- Date modifiied:
- 2019-04-23
Related products to: Human IL-17A (homodimer) ELISA kit
Related articles to: Human IL-17A (homodimer) ELISA kit
- Pyoderma gangrenosum (PG), a refractory inflammatory disorder, remains a condition with incompletely understood pathogenesis. Currently, no FDA-approved treatments are available. Janus kinase (JAK) inhibitors have been reported sporadically in case studies as effective treatments for PG. - Source: PubMed
Publication date: 2026/08/15
Liu WenqiPeng LuWang RupengFan JianyongChen LingShen Zhu - Pre-metastatic niches composed of mainly myeloid cells are recognized as critical for tumor metastasis. However, whether adaptive immune cells also play an important role in pre-metastatic niche formation remains to be explored. - Source: PubMed
Publication date: 2026/08/14
Kujawski MaciejMartincuks AntonsSong MihaeZhang ChunyanHuang RuiWang TianyiSenguttuvan RosemaryNakamura BradPalmer MichaelBacon Eliza RIhle KenaForman Stephen JShively John ERodriguez-Rodriguez LornaPriceman Saul JYu Hua - Disturbances of 24-hour or circadian rhythms imposed by everyday irregular work and/or social schedules have been linked to vascular disease, including ischemic stroke. Using an established shift work-like paradigm and preclinical model for ischemic stroke, we have shown that environment-induced circadian dysregulation exacerbates stroke outcomes differentially to a greater extent in male than female rats. Because more severe stroke outcomes and circadian rhythm disturbances have been linked to gut pathophysiology, the present study examined the effects of chronic shifts in the LD cycle on gut cytoarchitecture, microbiota composition, metabolites, and inflammatory mediators for evidence of corresponding sex differences. Two independent cohorts of adult (5-7mo) rats exposed for 50d to fixed or shifted (12hr advance/5d) LD 12:12 cycles were used to examine the effects of circadian dysregulation on: fecal microbiome composition in relation to stroke survival (Cohort 1); and gut morphology, metabolites and inflammatory mediators (Cohort 2). Circadian entrainment of activity rhythms was stable during exposure to fixed LD cycles but was severely disrupted in shifted LD rats. Relative to fixed LD controls, male but not female rats exposed to shifted LD cycles were distinguished by significant alterations in the composition of the gut microbiome including reduced alpha diversity, shifts in beta diversity and correlations between the abundance of beneficial gut bacteria and stroke survival. The effects of circadian dysregulation on gut microbiota were accompanied by evidence of pathologic gut morphology (i.e., shorter and blunted villi, crypt hyperplasia, disruption of tight junction proteins and gut barrier integrity), decreased circulating levels of the neuroprotective short-chain fatty acid butyrate, and elevated serum concentrations of endotoxin and proinflammatory cytokine IL-17A in shifted LD male rats. These results suggest that alterations in gut cytoarchitecture, microbiota, metabolites and inflammatory mediators may contribute to sex differences in the effects of circadian dysregulation on ischemic stroke outcomes. - Source: PubMed
Publication date: 2026/08/14
Barnum EllaTurck Jonathan LSouza Karienn AMani Kathiresh KumarPilla RachelSelvamani AmuthaSohrabji FaridaEarnest David J - Atopic dermatitis (AD) is a common inflammatory skin disease associated with epidermal barrier dysfunction, immune dysregulation, and microbial dysbiosis. Loss-of-function mutations in filaggrin, a critical epidermal protein, represent the strongest genetic risk factor for AD and result in compromised skin barrier integrity and altered immune responses. MyD88 is an adaptor protein essential for TLR and IL-1 receptor signaling, with dual roles in promoting inflammation and regulating immune tolerance. However, the function of MyD88 in maintaining skin homeostasis in the context of filaggrin deficiency remains unclear. Here, we used filaggrin-deficient (ft/ft) mice crossed with MyD88 knockout mice (ft/ftMyD88-/-) to investigate the immunological and microbial consequences of MyD88 signaling. In wildtype and ft/ft mice, MyD88 was predominantly expressed in skin epithelia during homeostasis, whereas ft/ftMyD88-/- mice developed spontaneous periocular skin inflammation. RNA-seq revealed upregulation of the IL-17 pathway in ft/ftMyD88-/- inflamed skin. Flow cytometry identified Vγ4 ⁺ γδ T cells as the major source of IL-17A in ft/ftMyD88-/- inflamed skin. We also discovered that ft/ftMyD88-/- skin inflammation was associated with markedly downregulated lipid metabolism genes as well as sebaceous gland abnormalities histologically. Moreover, 16S rRNA gene sequencing demonstrated microbial dysbiosis in ft/ft MyD88-/- periocular skin, which drove skin inflammation as well as IL-17-producing γδ T cell infiltration. Our findings indicate a role for MyD88 in homeostatic control of sebaceous glands and suppression of dysbiosis-driven IL-17A-mediated inflammation in filaggrin-deficient skin. These insights advance our understanding of AD pathogenesis and may offer novel therapeutic strategies for patients with filaggrin mutations. - Source: PubMed
Publication date: 2026/08/14
Wu Meng-JenRavipati AdvaitaaWang YuFeller Laine EChu AlyssaDamarla RishiLi ZhiyangTsoi Lam CGriffin RyleighHou PengLiang HaiGeha RaifSegre Julia AKong Heidi HGudjonsson Johann EArcher Nathan K - Although Rheumatoid arthritis (RA) management has improved substantially with modern pharmacological therapies, many patients still fail to achieve sustained treatment targets. This study investigated the therapeutic effects and potential mechanisms of asparagus polysaccharide (APS) in tumor necrosis factor-α (TNF-α)-induced MH7A cell dysfunction and collagen-induced arthritis (CIA) in mice. In vitro, MH7A cells were treated with different concentrations of APS, and cell viability, apoptosis, cell cycle distribution, and related protein and gene expression were assessed. In vivo, CIA model was established in mice, followed by APS administration. Paw volume, joint histopathology, serum cytokine levels, and the splenic Th17 cell proportion were evaluated. APS (≥ 3 mg/mL, 48 h) decreased MH7A cell viability. APS (3, 4, 5 mg/mL, 24 h) promoted apoptosis and inhibited proliferation in TNF-α-treated MH7A cells. APS (5 mg/mL, 24 h) downregulated Bcl-2 and cell cycle-related genes and suppressed NF-κB pathway activation. In the CIA mouse model, APS reduced paw volume, alleviated joint inflammation and tissue damage, decreased serum TNF-α, interleukin-6 (IL-6), IL-17A levels, increased IL-10 levels, and inhibited splenic Th17 cell expansion in a dose-dependent manner, without a significant effect on Treg cell proportion. APS exerts anti-arthritic effects in vitro and in vivo by regulating synoviocyte proliferation and apoptosis, inflammatory cytokine balance, and Th17 cell differentiation. The in vitro mechanism was associated with inhibition of NF-κB signaling. These findings provide preliminary experimental evidence supporting further investigation of APS as a candidate therapeutic agent for RA. - Source: PubMed
Publication date: 2026/08/14
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