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。警报素HMGB1介导固有免疫的作用日益引起重视，其在细胞外发挥警报素作用，与免疫细胞表面特定受体结合，对固有免疫和获得性免疫进行调节。本组前期实验发现HMGB1在真菌性角膜炎组织表达增强，角膜上皮细胞受到真菌刺激后，其胞浆转移，且培养液中含量增加。本研究采用真菌性角膜炎动物模型和角膜上皮细胞与致病真菌共培养体系，系统研究HMGB1及相关分子参与真菌性角膜炎发病机理，通过不同层次分别阻断或干扰HMGB1，判定其参与该疾病的相关机制，从宏观和微观角度了解HMGB1对病程的作用，为真菌性角膜炎发病机制提供实验依据。在此基础上通过抑制HMGB1的活性，减少其相关炎症因子的产生，降低真菌性角膜炎的炎症反应，为其生物治疗提供一种新思路。

Fungal infection of the eye are important diseases, even with keratoplasty, the prognosis is poor. And the incidence is raising nowaday in China, while the mechanism is not clear. Alarmin HMGB1 is one of the key proinflammatory factors in innate antifungal immunity, which was released from inflammatory cells, followed by combining with receptors, then regulated the innate and acquired immunity. Recently, we found that the expression of HMGB1 in keratitis tissue was upregulated, and in the culture media, the concentration was higher than that from the cultured human limbal epithelial cells when challenged by Candida albicans. This study systematically investigates the mechanism of HMGB1 involving in fungal keratitis, by corneal epithelial cells and fungi co-culture system and animal model, to block or interfere with HMGB1 from different levels, in order to analyze the mechanism of HMGB1 related molecules in fungal keratitis. And from macro and micro angles of view, we tend to understand its effect on the course of the disease and the mechanism for the pathogenesis of fungal keratitis. At the same time, our aim is by inhibiting the activity of HMGB1 and reducing the production of related inflammatory factors, to reduce the inflammatory reaction of corneal tissue. If achieved, the role of HMGB1 in host anti-fungal defence and inflammatory response during fungal keratitis will be well established. And this study will afford a novel therapeutical benefit in the treatment of fungal keratitis.