真菌性角膜炎是较常见的难治性致盲眼病，发病率在我国有上升趋势，即使联合角膜移植手术，预后仍较差，其发病机制尚不清楚。NLRP6炎症小体是近年固有免疫研究的热点，其在真菌性角膜炎发病过程中作用的研究尚未见报道。本组前期实验发现角膜上皮细胞在致病真菌刺激后NLRP6表达降低，加入NLRP6重组蛋白后炎症小体相关分子IL-1β、IL-18和抗微生物蛋白LL-37表达增高，某些炎症因子亦表达降低，受损角膜上皮修复能力增强。本研究拟采用共培养体系和真菌性角膜炎动物模型，系统探讨NLRP6相关因子参与真菌性角膜炎发病机理，验证其在疾病过程中发挥杀灭真菌、抗炎和角膜上皮修复等多重效应。通过改变NLRP6分子活性，判定其参与疾病过程中的相关免疫学分子机制，从宏观和微观角度了解其对疾病进程的作用，为真菌性角膜炎发病机制提供实验依据，为真菌性角膜炎的生物治疗提供一新思路。

Fungal infection of the eye is an important disease, even with keratoplasty, the prognosis is poor. And the incidence is raising nowadays in China, while the mechanism is not clear. NLRP6 inflammasome is a hotspot in innate immunity research in recent years, while the research on its role in the pathogenesis of fungal keratitis is still blank. Our previous experiments showed that the expression of NLRP6 decreased after stimulation by pathogenic fungi. After adding NLRP6 recombinant protein, the expression of NLRP6 inflammasome related molecules IL-1beta, IL-18 and anti-microbial protein LL-37 increased, while the inflammatory cytokine TNF-alpha decreased, and the repair ability of damaged corneal epithelium improved. In this study, co-culture system and fungal keratitis animal model will be used to systematically explore the role of NLRP6 related molecules in the pathogenesis of fungal keratitis, and to verify its multiple effects of fungicidal, anti-inflammatory and corneal epithelial repair in the course of disease. By regulating the activity of NLRP6 molecule, we will try to discover the relevant immunological molecules involved in the process of disease, and understand the role of NLRP6 molecule in the process of disease, so as to provide experimental basis for the pathogenesis of fungal keratitis. Moreover, by increasing the activity of NLRP6 to enhance its multiple effect function, it would provide a new strategy for the biological treatment of fungal keratitis.