An estrogen-independent and IL-1-dependent pathway controls vulvovaginal candidiasis through combined IL-17/IL-22 signaling.

ABSTRACT: Vulvovaginal candidiasis (VVC), caused by the commensal pathobiont Candida albicans, affects >75% of women, marring quality of life and incurring significant health costs. Estrogen (E2) activity is tightly linked to VVC susceptibility, and preclinical models employ E2 to establish vaginal colonization. Unlike most forms of candidiasis, VVC is not considered to be a condition of immune compromise. Rather, VVC is characterized by high levels of PMNs and inflammatory cytokines that drive immunopathology but fail to clear the fungus. The role of the Type 17 pathway in this condition is controversial. Th17 signature profiles are upregulated in vaginal tissue during VVC in mice and humans. However, loss of individual Th17 components by gene deletion or anti-cytokine administration does no

SUBMITTER: Coleman BM 

PROVIDER: S-EPMC12407711 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature