Ask about this productRelated genes to: IL17A antibody
- 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: IL17A antibody
Related articles to: IL17A antibody
- Commensal microbes can cause invasive infection but can also stimulate protective immune responses as exemplified by the gut pathobiont Candida albicans. This species primes systemic Th17 immunogenicity which protects against disseminated infection, and yet the fungal determinants driving protection remain uncertain. Here we show an essential role for the cytolytic toxin candidalysin for C. albicans colonization-induced systemic Th17 immunogenicity and protection against invasive infection. Mice intestinally colonized with candidalysin-deficient cells show reduced accumulation of CD4 T cells with defined fungal specificity, despite similar intestinal colonization levels to wildtype C. albicans cells. Fungal-specific RORγt + CD4 T cells are particularly reduced together with their production of IL17A and IL17F cytokines, whereas expression of transcription factors and production of cytokines representative of other helper T cell lineages are unaffected. Protection against fungemia conferred by colonization with wildtype C. albicans is absent from mice colonized with candidalysin-deficient cells as shown by increased fungal pathogen burden and reduced survival after intravenous infection. These results establish the necessity for candidalysin for priming Th17 fungal-specific adaptive immune cells and highlight paradoxical protective roles for this fungal virulence factor for promoting host defense against invasive systemic disease. - Source: PubMed
Publication date: 2026/05/07
Nguyen Ngan N MBrady Alexander EHaslam David BFrazer CoreyPham GiangBennett Richard JWay Sing Sing - The global poultry industry incurs substantial economic losses due to Salmonella enterica serovar Enteritidis (S. Enteritidis), underscoring the urgent need for cross-protective vaccines capable of addressing evolving pathogen diversity. Using an integrative vaccinology approach, we systematically screened immunoreactive proteins to identify novel subunit vaccine candidates. Eight candidate proteins, including type III secretion system components (SipA, SopE2, SipB, SipC), membrane-associated proteins (TolA, TolC, LamB), and the virulence factor MipA, demonstrated pronounced antigenic and immunogenic properties. Further investigation revealed that SipC and TolC induced balanced Th1/Th2 responses and IL-17A secretion, contributing to multifaceted immunity. Opsonophagocytic assays demonstrated that antisera against SipC and TolC significantly enhanced neutrophil-mediated killing of homologous and heterologous strains. Notably, antisera against SipC exhibited enhanced efficacy in promoting neutrophil killing of the heterologous UK-1 strain. In challenge studies, SipC provided 66.7 % protection against a homologous strain and demonstrated 50 % cross-protection against the UK-1 strain, thereby exhibiting superior efficacy compared to other candidate antigens. Both antigens significantly decreased bacterial loads in visceral organs following challenge. This study identifies SipC, and to a lesser degree TolC, as potential broad-spectrum subunit vaccine antigens, providing a foundation for next-generation poultry salmonellosis vaccines with extensive protective efficacy. - Source: PubMed
Publication date: 2026/05/01
Zhao YuyingLi GuohuiLi Yu-AnLi QuanShi Huoying - Psoriasis is associated with elevated cardiovascular risk, partly mediated through dyslipidemia and the interleukin-23/Th17 inflammatory axis. Interleukin-17A (IL-17A) inhibitors demonstrate superior dermatologic efficacy, but their effects on lipid metabolism remain controversial. Most previous studies analyzed lipid changes at the population level without stratifying by baseline lipid phenotypes. This study aimed to evaluate the phenotype-specific effects of IL-17A inhibitors on lipid profiles and identify risk factors for dyslipidemia in moderate-to-severe plaque psoriasis. - Source: PubMed
Publication date: 2026/05/09
Wu ChaoWang Si-FanLi Dian-MoHe Chun-XiaJin Hong-Zhong - Psoriasis is a chronic skin disease characterized by keratinocyte hyperproliferation and inflammation, largely driven by the cytokines IL-22 and interferon (IFN)-γ. These cytokines activate the signal transducer and activator of transcription (STAT) 3 and STAT1 molecular pathways, leading to abnormal proliferation, impaired differentiation, and increased production of inflammatory mediators in keratinocytes. While the IL-22/STAT3 pathway primarily promotes de-differentiation in keratinocytes, IFN-γ/STAT1-3 signaling induces pronounced inflammation, despite exerting antiproliferative effects on these cells. Recent research has highlighted the role of serine/glycine metabolism in the pathogenesis of psoriasis, by supporting T cell and keratinocyte proliferation. Furthermore, pharmacological inhibition of serine catabolism through targeting serine hydroxymethyltranferase (SHMT)1/2 enzymes reduced the infiltration of inflammatory cells in the skin of the imiquimod-induced mouse model of psoriasis. This study investigates the role of serine catabolism in psoriasis, focusing on its influence on keratinocyte proliferation and inflammation. We examined how pharmacological inhibition of SHMT1/2, mediated by a folate-competitive cell-permeable inhibitor Serine Hydroxymethyltransferase INhibitor 1 (SHIN1), affects keratinocyte proliferation and inflammatory signaling pathways in response to psoriasis-associated cytokines IL-22 and IFN-γ, using both in vitro and ex vivo models of the disease. We found that SHIN1 reduced keratinocyte proliferation, particularly under IL-22 stimulation, and restored differentiation in ex vivo psoriasis skin explants by reversing the effects of IL-22. SHIN1 also inhibited IFN-γ-induced expression of pro-inflammatory genes (e.g., CXCL10, CXCL9, CCL5, CCL2, IL-6) and reduced STAT3 activation, with only modest effects on STAT1 and extracellular signal-regulated kinase 1/2 activation. In psoriasis explants, SHIN1 decreased the expression of Ki67, Keratin 16, and pro-inflammatory cytokines including IL-17A, IL-22, and IFN-γ. These findings support the therapeutic potential of SHIN1 as a metabolism-targeted agent for psoriasis and other cytokine-mediated skin disorders, providing a rationale for further exploration of novel treatment strategies. - Source: PubMed
Publication date: 2026/05/08
Mercurio LauraDi Francesco ValentinaSergio SimoneMorelli MartinaScarponi ClaudiaMadonna StefaniaPallotta SabatinoMancini MaraCappello AngelaCandi EleonoraAlbanesi Cristina - Ischemic stroke is a leading cerebrovascular disorder frequently complicated by cerebral ischemia-reperfusion injury (CIRI), which aggravates neurological damage and worsens clinical outcomes. Yangyin Formula (YYF), a traditional Chinese medicine composed of Rehmannia glutinosa, Dendrobium officinale, and Pueraria lobata, has shown potential in mitigating CIRI. To elucidate its therapeutic mechanisms, we integrated network pharmacology, molecular docking, and molecular dynamics simulations, followed by in vivo validation in a rat model of middle cerebral artery occlusion/reperfusion (MCAO/R). A total of 61 bioactive compounds and 768 targets were identified, enriched in 136 signaling pathways. Computational analyses revealed strong binding affinities between key YYF components and CIRI-related targets. In vivo, YYF administration significantly improved neurological function, reduced infarct volume, and alleviated histopathological damage. Furthermore, YYF suppressed IL-17A, TNF-α, IL-1β, Caspase-3, p38 MAPK, and NF-κB p65 expression in brain and serum, with effects comparable to IL-17A inhibition. These findings suggest that YYF exerts neuroprotective effects against CIRI by modulating the IL-17A/p38 MAPK/NF-κB p65 signaling pathway, highlighting its potential as a therapeutic strategy for ischemic stroke. - Source: PubMed
Publication date: 2026/05/08
Shi KunWan HaofangHan JinYang JiehongWan Haitong