The IL-17A/TNFSF10 axis promotes vulvovaginal candidiasis pathogenesis by inducing neutrophil necroptosis.

Authors

Mingkun Shao, Wanqin Hu, Hongxiao Feng, Sainan Li, Wenjin Qi, Yang Liu

Published in

Frontiers in cellular and infection microbiology. Volume 16. Pages 1910964. Epub Sep 24, 2026.

Abstract

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.
Clinical specimens, RNA sequencing, cell-based assays, and mouse models were used.
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.
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.

PMID:
42851347
Bibliographic data and abstract were imported from PubMed on 09 Oct 2026.

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