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
- Bimekizumab, a dual IL-17A and IL-17F inhibitor, has demonstrated high efficacy in moderate- to-severe psoriasis in clinical trials. However, real-world evidence in patients with moderate disease remains limited. - Source: PubMed
Publication date: 2026/07/01
Feresin FrancescaBernardini NicolettaCampione ElenaCaldarola GiacomoGubinelli EmanuelaMoretta GaiaPagnanelli GianlucaGiordano DomenicoPersechino SeverinoFalco Gennaro MArtosi FabioZappia ElenaPellacani GiovanniPotenza ConcettaRichetta Antonio GiovanniDe Simone ClaraOrsini DiegoDattola Annunziata - To investigate the impact of hyperglycemia and systemic inflammation on experimental periodontitis/peri-implantitis in diabetic mice, focusing on osteoimmunological dysregulation and oral microbial alteration. - Source: PubMed
Publication date: 2026/06/24
Memida TakumiJaar Jacques ChristopherChen TsuteCao GuoqinKuriki NanakoAbdolahinia Elaheh DalirOkamoto MotokiShindo SatoruYamashita ShoheiHe XuesongSuzuki MaikoVardar SaynurKawai ToshihisaHan Xiaozhe - This study evaluated the effects of live and heat-killed HP7 on intestinal motility, host physiological responses, and gut microbiota in a mouse model of delayed intestinal transit. BALB/c mice were treated with live HP7 (HP7L), heat-killed HP7 (HP7K), or bisacodyl following loperamide administration. HP7L and HP7K improved intestinal motility-related parameters, including fecal output, stool consistency, fecal moisture content, and charcoal meal transit. HP7 treatment also modulated circulating gastrointestinal hormones and inflammatory cytokines, with changes in serotonin, ghrelin, peptide YY, IL-6, and IL-17A. In intestinal tissues, HP7 regulated the expression of genes related to neuroendocrine signaling, water transport, mucus production, and tight junction integrity, including and . Histological analysis further showed reduced colonic tissue alterations and improved structural parameters. Microbiota analysis revealed that HP7L exerted broader effects on microbial community structure, whereas HP7K induced more selective taxonomic changes. Predicted functional profiling suggested that both HP7L and HP7K were associated with shifts in carbohydrate metabolism-related pathways, with HP7K showing additional predicted enrichment of pathways related to redox-associated metabolism, lipid metabolism, and microbial substrate utilization. These findings suggest that heat-killed HP7 retains biological activity and has potential as a postbiotic candidate for regulating intestinal motility. - Source: PubMed
Publication date: 2026/07/01
Gwon HyeonjunKim HyeonjiKim Joo-YunShim Jae-JungLee Jae-Hwan - Ischemia-reperfusion injury (IRI) and acute cellular rejection (ACR) are common post-operative complications that lead to poor outcomes in lung transplant recipients. The transient receptor potential vanilloid 4 (TRPV4) is a plasma membrane Ca channel that controls vascular tone and integrity. We examined whether TRPV4 influences IRI and alloimmune responses in a mouse model of orthotopic lung transplantation. Recipients receiving syngeneic lungs briefly treated with a TRPV4-specific inhibitor, or engrafted with syngeneic lungs with an endothelial cell-specific TRPV4 gene ablation (TRPV4), had better graft function, reduced endothelial cell adhesion molecule expression, and lower inflammatory cytokine expression and neutrophil recruitment. TRPV4 lungs transplanted into immunosuppressed, major MHC-mismatched recipients had more intragraft CD25 Foxp3 CD4 T cells and fewer IFN-γ CD8 T cells and were more resistant to IRI-induced ACR when compared to wildtype allografts. Finally, pharmacological inhibition of TRPV4 reduced donor-antigen-triggered production of IFN-γ and IL-17A by intragraft T cells and prevented ACR despite IRI. Our findings show that pulmonary endothelial cell TRPV4 activity couples ischemic tissue injury to T cell alloimmunity, highlighting the potential of therapies that enhance vascular integrity to promote transplant tolerance. - Source: PubMed
Publication date: 2026/07/08
Liao FuyiTa Huy QZhou DequanDavis VictoriaCano MarleneKrupnick Alexander SKreisel DanielSonkusare Swapnil KLaubach Victor EGelman Andrew E - Drug-induced liver injury remains a major cause of clinical trial attrition and postmarketing drug withdrawals, reflecting persistent translational gaps in predictive preclinical models of compound hepatotoxicity. Here, we applied a well-characterized 3-dimensional primary human liver spheroid platform to interrogate diverse mechanisms of hepatotoxicity and benchmark performance against recent real-world clinical cases. After multicenter technology transfer, spheroids maintained stable hepatic functionality, including expression of metabolic enzymes and transporters, albumin secretion, and long-term CYP activity. Importantly, repeated-dose exposure to established hepatotoxins demonstrated robust, concentration-dependent toxicity with excellent interexperimental (R = 0.98) and interdonor (R = 0.89) reproducibility. To resolve toxicity mechanisms, we implemented Seahorse extracellular flux analysis in liver spheroids, which enabled sensitive detection of early mitochondrial dysfunction, allowing mechanistic discrimination between mitochondrial and nonmitochondrial toxins. Cholestatic liability was identified using bile acid coexposure with accurate classification of chlorpromazine and bosentan and confirmation of bile salt export pump downregulation. Importantly, the model also recapitulated hepatotoxicity signals observed in recent clinical development, including for Bruton's tyrosine kinase inhibitors (tolebrutinib and evobrutinib), oral glucagon-like peptide-1 receptor agonists (danuglipron vs orforglipron), synergistic toxicity on azelaprag-tirzepatide coexposure and enhanced sensitivity to the IL-17A inhibitor LY3509754 on coculture with nonparenchymal liver cells. Collectively, we present new assays for the mechanistic resolution of hepatotoxicity and provide further evidence that 3-dimensional human liver spheroids enable reproducible, mechanistically informative, and clinically aligned assessment of drug-induced liver injury across multiple modalities, which supports their application for preclinical de-risking of drug candidates. SIGNIFICANCE STATEMENT: This study shows that primary human liver spheroids provide a reproducible and mechanistically informative platform for preclinical assessments of drug metabolism and liver toxicity. The model maintains stable CYP expression and metabolic activity, captures the impact of nonparenchymal cells on hepatic clearance, and detects mitochondrial, cholestatic, and interaction-driven toxicity, including recent real-world clinical cases. These findings support 3-dimensional human liver spheroids as translational new approach methodologies for integrating metabolism and toxicity in drug development. - Source: PubMed
Publication date: 2026/06/22
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