摘要
系统性红斑狼疮是临床表现复杂、发病率较高的自身免疫性疾病。本病基本特征是自身抗原耐受性降低及自身抗体的产生。由于中性粒细胞死亡途径的改变,包括凋亡、继发坏死(SNECs)、中性粒细胞胞外捕获网(NETs)形成,凋亡细胞清除受损、含核DNA的NETs降解不全,继发坏死细胞(SNECs)释放出自身抗原。而修饰后的自身抗原经由滤泡树突状细胞(FDC)提呈给自身反应性B细胞,导致自身免疫耐受突破和自身抗体产生。自身抗体和未被清除的细胞碎片形成的免疫复合物(IC)沉积在循环组织,合并机体清除IC过程中产生的大量促炎因子导致系统性红斑狼疮(SLE)持续不断的炎症反应和组织损伤。本文就中性粒细胞凋亡形成、凋亡清除及清除受损在SLE发病机制中的研究进展做一综述。
Systemic lupus erythematosus （SLE） is a prototype inflammatory autoimmune disease, which has com- plex clinical appearance and high morbidity. A characteristic hallmark of SLE is production of autoantibodies against nu- clear components and breaking immunological tolerance. Because of neutrophils death pathways change, including apop- tosis, SNECs, NETosis, autoantigens are mainly released from secondary necrotic cells （SNECs）. These modified au- toantigens are presented by follicular dendritic cells to autoreactive B cells, then results in breaking of self-tolerance and production of autoantibodies. The clearance of immune complex （IC）, along with the accumulation of cell remnants re- presents an initiating event of the etiology. The subsequent generation of autoantibodies results in perpetuating inflamma- tion and tissue damage in SLE patients. This review elaborated pathogenesis of SLE, emphasis on the process of neutro- phil apoptosis, clearance of apoptotic cells and defective clearance, and look forward to the new treat-target in SLE.
出处
《西部医学》
2017年第7期1018-1022,共5页
Medical Journal of West China
基金
国家自然科学基金(2014HH0027
20120181110009)
