程序性细胞死亡途径在系统性红斑狼疮炎症和免疫反应中的作用机制  

Mechanism of programmed cell death pathway in systemic lupus erythematosus inflammation and immune response

作　　者：李媛[1] LI Yuan(Department of Rheumatology and immunology,Tianjin the First Central Hospital,Tianjin 300190,China)

机构地区：[1]天津市第一中心医院风湿免疫科,天津300190

出　　处：《医药论坛杂志》2023年第4期108-112,共5页Journal of Medical Forum

摘　　要：系统性红斑狼疮(systemic lupus erythematosus, SLE)是一种异质性自身免疫性疾病,其特征是过度炎症和免疫反应造成的组织损伤。程序性细胞死亡包括细胞凋亡、继发性坏死、细胞焦亡、坏死性凋亡和自噬等不同形式的溶解性细胞死亡,越来越多的证据表明了程序性细胞死亡途径在SLE发病中的重要作用。当清除缺陷时,累积的凋亡细胞导致继发性坏死。损伤相关分子模式(damage associated molecular pattern, DAMP)和自身抗原的释放,引发SLE的免疫和组织损伤。而自噬在SLE发病机制中的作用仍有争议。本综述简要讨论了不同形式的程序性细胞死亡途径在SLE炎症和免疫反应中的作用机制。Systemic lupus erythematosus(SLE) is a heterogeneous autoimmune disease, which is characterized by tissue damage caused by excessive inflammation and immune response. Programmed cell death includes apoptosis, secondary necrosis, focal death, necrotic apoptosis and autophagy. More and more evidence shows the important role of programmed cell death pathway in the pathogenesis of SLE. When the defect is cleared, the accumulated apoptotic cells lead to secondary necrosis. Damage associated molecular pattern(DAMP) and the release of autoantigens lead to immune and tissue damage in SLE. The role of autophagy in the pathogenesis of SLE is still controversial. This review briefly discusses the mechanism of different forms of programmed cell death pathway in SLE inflammation and immune response.

关 键 词：程序性细胞死亡途径 系统性红斑狼疮 发病机制 细胞凋亡 

分 类 号：R593.241[医药卫生—内科学]