ITGAX promotes Th17-cell differentiation and drives pathogenesis in pediatric ulcerative colitis.

BACKGROUND: Pediatric ulcerative colitis (UC) is an inflammatory bowel disease characterized by dysregulated immune responses and intestinal inflammation, often more severe than adult-onset UC. Th17 cells play a crucial role in UC pathogenesis but the mechanisms regulating their differentiation and recruitment in pediatric UC remain incompletely understood. METHODS: Th17 differentiation assays with siRNA knockdown and an in vivo dextran sodium sulfate (DSS)-induced UC mouse model with intrarectal siRNA administration. RESULTS: Th17 cells in the colon. CONCLUSION: ITGAX is a key promoter of Th17-cell differentiation and expansion, contributing to the pathogenesis of pediatric UC. Targeting ITGAX may represent a potential therapeutic strategy for pediatric UC by modulating aberrant Th17 responses.