补体系统在葡萄膜炎发病机制中的作用

Role of complement system in the pathogenesis of uveitis

葡萄膜炎是一组累及虹膜、睫状体、脉络膜、玻璃体、视网膜及视网膜血管的炎症性疾病,可造成视力减退甚至视力丧失。葡萄膜炎的发病机制复杂多样,如感染、自身免疫、创伤及理化损伤、免疫遗传机制等。近年有研究表明,补体系统的激活是葡萄膜炎的发病机制之一,多种补体蛋白包括CFH、CFB、CFI、MAC、CD59等通过严密的机制调控补体系统介导的宿主组织损伤,研究发现补体蛋白在基因层面和生物学功能等方面参与了葡萄膜炎的发生发展。另外C2、C3、C4、C5等补体成分在拷贝数变异、基因多态性及调节T细胞反应介导自身免疫发展等方面影响葡萄膜炎的发病机制。因此,补体抑制疗法和相关基因疗法为葡萄膜炎的治疗提供了新的思路及作用靶点。

Uveitis is a group of inflammation diseases involving the iris, ciliary body, choroid, vitreous body, retina and retinal vessels, which can lead to visual deterioration and even visual loss. The pathogenesis of uveitis is complex and diverse, including infection, autoimmunity, trauma, physical and chemical injury, immune genetic mechanism and so on. Recent studies have shown that the activation of complement system is one of the pathogenesis of uveitis. Various complement proteins, including CFH, CFB, CFI, MAC, CD59 and so on, regulate host tissue damage through a rigorous mechanism mediated by the complement system. And studies have found that those complement proteins are involved in the occurrence and development of uveitis at the gene level and biological function. In addition, complement components like C2, C3, C4 and C5 can affect the pathogenesis of uveitis in terms of copy number variation, gene polymorphism and the regulation of T-cell-mediated autoimmune response. Therefore, complement inhibition therapy and related gene therapy provide new ideas and targets for the treatment of uveitis.