Candidalysin是近期发现的白色念珠菌分泌的细胞溶解型肽毒素，在角膜免疫炎症反应中的作用机理尚无报道。本课题组前期研究证实白色念珠菌能够激活TREM-1发挥炎症放大作用，且外源性Candidalysin能够诱导TREM-1表达。为此我们提出假说：白色念珠菌感染角膜上皮后释放Candidalysin，进而调控TREM-1/DAP12信号通路实现其生物学效应。本研究以小鼠角膜炎动物模型、人角膜上皮细胞系和患者角膜组织标本为研究对象，采用基因敲除、Real time PCR、Western blot、FACS、ELISA、免疫荧光等研究方法，从分子、细胞、组织以及动物水平探讨TREM-1在Candidalysin触发角膜炎症中的作用，明确Candidalysin通过TREM-1/DAP12信号通路触发角膜免疫炎症反应的调控机制，为白色念珠菌性角膜炎的防治提供新的理论和实验依据。

Candidalysin is a cytolytic peptide toxin secreted by Candida albicans. While its role and mechanism in corneal immune inflammation remain unknown. We identified that Candida albicans can activate the TREM-1 to exert an inflammatory amplification effect. Notably, we also discovered that exogenous Candidalysin can induce TREM-1 expression. Therefore, we propose a hypothesis: Candidalysin is released after infection of the corneal epithelium by Candida albicans, and its biological effects are achieved by regulating the TREM-1/DAP12 signaling pathway. In this study, a keratitis model in mice, human corneal epithelial cell line and patients' corneal specimens were used. Gene knockout, Realtime PCR, Western blot, FACS, ELISA, immunofluorescence and other research methods were examined to explore the pivotal role of TREM-1 in the corneal inflammation triggered by Candidalysin through the molecular, cellular, tissue and animal levels. Our study provides evidence that Candidalysin triggers corneal immune inflammation by modulating TREM-1/DAP12 signaling. The study of Candidalysin and TREM-1 can provide new insights on the treatment of Candida albicans keratitis through the experimental results and theoretical predictions.