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Table · dataset · 2026

Data Sheet 1_The IL-17A/TNFSF10 axis promotes vulvovaginal candidiasis pathogenesis by inducing neutrophil necroptosis.pdf

Listed in figshare and Loughborough Research Repository — shown once because both records carry DOI 10.3389/fcimb.2026.1910964.s002

Introduction<p>Vulvovaginal candidiasis (VVC) is a common infection of the female reproductive tract and is closely associated with dysregulated mucosal immunity.

Description

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>

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Inferred from text
RNA sequencing 75% · Sequencing 75%
Provenance · 2 source records, 32 field assertions
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