Ⅰ型干扰素在系统性红斑狼疮发病中过度激活的机制

Mechanism of Type Ⅰ Interferon Overactivation in Pathogenesis of Systemic Lupus Erythematosus

在正常免疫应答过程中,干扰素(IFN)在机体内起到防御病毒的作用。Ⅰ型干扰素(Ⅰ-IFN)作为IFN的重要组分之一,可能在多种自身免疫性疾病发病中发挥重要作用,如系统性红斑狼疮(SLE)、类风湿关节炎、干燥综合征等。SLE是一种病因复杂,累及多组织、多器官的自身免疫性疾病。Ⅰ-IFN系统过度激活可能是SLE发病的原因之一,其机制主要包括Ⅰ-IFN诱导剂的存在、Ⅰ-IFN通路基因组成的异质性以及产生Ⅰ-IFN细胞的异常激活。鉴于Ⅰ-IFN在SLE中的重要作用,已将其作为治疗靶标进行相关药物的研发。

In normal immune responses,interferons( IFNs) have a critical role in the defense against viruses in the body. As one of the important components of interferons,type Ⅰ interferons( Ⅰ-IFN) is involved in the pathogenesis of a variety of autoimmune diseases including systemic lupus erythematosus( SLE),rheumatoid arthritis and Sjogren syndrome.SLE is an autoimmune disease with complex etiology involving multiple tissues and multiple organs. Over-activation of theⅠ-IFN system may be one of the causes of SLE,and its mechanisms mainly include the existence of Ⅰ-IFN inducers,heterogeneity of Ⅰ-IFN pathway gene composition,and activation of several IFN-producing cells. In view of the important role of Ⅰ-IFN in SLE,it has been used as a therapeutic target for the research and development of related drugs.