葡萄膜炎是Treg/Teff失衡介导的自身免疫性、高致盲眼病。提高Treg数量或增强其功能是治疗关键。既往研究显示，LncRNAs可作为海绵吸附体竞争性结合miRNAs，调控其靶基因mRNA编码蛋白能力，参与疾病发生发展。我们前期通过基因芯片筛选出自身免疫性葡萄膜炎（EAU）小鼠和正常小鼠差异表达的LncRNAs和miRNAs，进行生物信息分析及功能鉴定，确定人鼠同源目标LncRNA AK005410（↑）,其序列中与候选miRNA miR-145a-5p（↓）有3个结合位点且能竞争性结合；且miR-145a-5p的靶基因RUNX1,具有调控T细胞分化的功能。本课题拟通过基因敲除、慢病毒转染、siRNA沉默等技术，探讨LncRNA AK005410/miR-145a-5p/RUNX1通过调节Treg分化、功能和稳定性参与葡萄膜炎发生发展机制，并进行临床验证，为葡萄膜炎的诊疗提供科学依据。

Uveitis is an autoimmune eye disease of high probability of causing blind, which is mediated with Treg/Teff imbalance. Increasing the number of Treg or enhancing its function is the key to successful treatment. Previous studies indicate that LncRNAs could act as sponge to compete for miRNAs which are supposed to binding to mRNA targets, thus regulate protein-coding and participate in the progress of diseases. We have identified differential expressed LncRNA (AK005410 ↑) and miRNA (miR-145a-5p ↓)between Experimental Autoimmune Uveitis and normal control via microassays and comprehensive analysis, moreover, LncRNA AK005410 has 3 binding sites and could interact with miR-145a-5p . After searching for predicted miR-145a-5p targets in several online databases, and we identified RUNX1 which was critically involved in biological process of T cell differentiation , was the target of miR-145a-5p. Here, we aim at investigate AK005410/miR-145a-5p/RUNX1 in the pathogenesis of uveitis via regulating Treg cells, and provide scientific evidence for diagnosis and therapy.