外阴阴道假丝酵母菌病(VVC)的顽固复发与真菌生物膜感染是临床难题之一。目前国内外对VVC免疫学机制的研究已转移至阴道上皮细胞(VEC)的固有免疫应答，具体机制尚未完全阐明。近期我们研究发现，真菌群体感应信号分子farnesol除了能抑制真菌粘附、菌丝及生物膜的形成外，还能增强阴道固有免疫应答，上调干扰素基因刺激蛋白(STING)的表达，推测farnesol可能通过固有免疫应答STING-TBK1-IRF3信号通路调控VEC抗真菌的免疫应答，间接调控适应性免疫应答。本项目拟在此基础上深入研究，采用RNA干扰或过表达技术等，利用细胞培养系统或模型动物，分析STING上下游因子及靶效应分子I型干扰素(IFN-α/β)表达变化，进一步分析farnesol及STING通路在阴道局部免疫应答中的作用及机制，为farnesol及STING-TBK1-IRF3信号通路在女性微生态领域中的应用提供新思路。

Recalcitrant recurrence and biofilm infections are one of the clinical problems of vulvovaginal candidiasis (VVC). At present, studies on the immunological mechanism of VVC have shifted the focus on the innate immune response of the vaginal epithelial cells (VEC), while its exact function and regulating mechanisms have not been elucidated. Recently, we have found that quorum sensing molecule farnesol could not only suppress fungal hyphae formation and adhesion, biofilm formation, but also could enhance vaginal innate immune response, upregulating Stimulator of interferon gene (STING). We speculate farnesol may regulate the VEC antifungal immune response via innate immune response related STING-TBK1-IRF3 signaling pathway, indirectly mediating the adaptive immune response. Based on the previous study, we plan to use RNA interference or overexpression technologies, cell culture system and animal models, analyzing the expression of downstream key factors and target effector molecules of STING-type I interferon (IFN-α/β), further revealing the role of farnesol and STING signaling pathway in vaginal local immune responses, providing a new theoretical basis for the application of farnesol and STING-TBK1-IRF3 signal pathway in female microecology.