Frontiers in cellular and infection microbiology · 2026
The IL-17A/TNFSF10 axis promotes vulvovaginal candidiasis pathogenesis by inducing neutrophil necroptosis.
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Shao Mingkun, Hu Wanqin, Feng Hongxiao, Li Sainan, Qi Wenjin, Liu Yang
Аннотация
INTRODUCTION: 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.
METHODS: Clinical specimens, RNA sequencing, cell-based assays, and mouse models were used.
RESULTS: 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.
DISCUSSION: 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.
METHODS: Clinical specimens, RNA sequencing, cell-based assays, and mouse models were used.
RESULTS: 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.
DISCUSSION: 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.