摘要
中性粒细胞胞外诱捕网(NETs)由DNA和抗菌蛋白质组成。在活细胞内,这些组分分布于亚细胞并发挥不同的功能。但是,在NETosis期,这些组分重新分布并从中性粒细胞内挤压出来。NETosis过分强盛和NETs清除受损,与自身免疫性疾病的器官损害有关,如系统性红斑狼疮(SLE)、类风湿性关节炎(RA)、Felty's综合征(FS)和小血管炎(SVV)等。NETs可能是体内新抗原的重要来源,蛋白质翻译后的修饰与水解,或药物诱导NETs构象异常能促进自身免疫性疾病患者产生自身抗体。总之,NETs可能提供了一个独特的具有破坏正常免疫耐受,引起自身免疫性的微环境。
Neutrophil extracellular traps （NETs） are composed of DNA and antimicrobial proteins. These components have diverse functions and subcellular distributions in live cells, which are redistributed and extruded from neutrophils by a death program termed NETosis. Both exuberant NETosis and impaired clearance of NETs have been implicated in the organ damage of autoimmune diseases, such as systemic lupus erythematosus （SLE）, rheumatoid arthritis （RA）, Felty＇s syndrome （FS）, small vessel vasculitis （SVV）, and so on. NETs may represent an important source of neoantigens, where posttranslational modifications and proteolytic cleavage of proteins externalized in the NETs, or abnormal conformation of drug-induced NETs, could promote the generation of autoantibodies in patients with autoimmune diseases. In short, NETs may provide a unique, stimulatory microenvironment that can break normal immune tolerance, and thereby predispose to autoimmunity.
出处
《分子诊断与治疗杂志》
2014年第1期62-65,共4页
Journal of Molecular Diagnostics and Therapy
