2026-10-14T03:37:29Z https://api.figshare.com/v2/oai

oai:figshare.com:article/33979717 2026-09-24T04:41:48Z category_303 portal_316 item_type_3 month_year_09_2026

Data Sheet 1_The IL-17A/TNFSF10 axis promotes vulvovaginal candidiasis pathogenesis by inducing neutrophil necroptosis.pdf Mingkun SHAO (25102114) Wanqin HU (25102117) Hongxiao FENG (25102120) Sainan LI (25102123) Wenjin QI (25102126) Yang LIU (10045196) Clinical Microbiology interleukin-17A necroptosis neutrophils TNFSF10 vulvovaginal candidiasis Introduction<p>Vulvovaginal candidiasis (VVC) is a common infection of the female reproductive tract and is closely associated with dysregulated mucosal immunity. This study investigated how IL-17A/TNFSF10 signaling regulates neutrophil death and VVC progression.</p>Methods<p>Clinical specimens, RNA sequencing, cell-based assays, and mouse models were used.</p>Results<p>IL-17A enhanced neutrophil extracellular trap formation and increased TNFSF10/TNFRSF10 expression, together with increased phosphorylation of RIP3 and MLKL. In vivo, IL-17A aggravated mucosal injury and neutrophil infiltration, whereas TNFSF10 manipulation altered neutrophil accumulation, inflammatory responses, and epithelial barrier function.</p>Discussion<p>These findings suggest that IL-17A/TNFSF10 signaling contributes to neutrophil death, mucosal inflammation, and VVC progression. Targeting this pathway may represent a potential therapeutic strategy for VVC.</p> 2026-09-24T04:41:48Z Dataset Dataset 10.3389/fcimb.2026.1910964.s002 https://figshare.com/articles/dataset/Data_Sheet_1_The_IL-17A_TNFSF10_axis_promotes_vulvovaginal_candidiasis_pathogenesis_by_inducing_neutrophil_necroptosis_pdf/33979717 CC BY 4.0