Neutrophil Extracellular Traps and Systemic Lupus Erythematosus.
Neutrophil Extracellular Traps and Systemic Lupus Erythematosus.
复制标题
DOI：
10.4172/2155-9899.1000139
复制
发表时间：
2013-04
期刊：
影响因子：
--
通讯作者：
Yangsheng Yu;K. Su
中科院分区：
文献类型：
--
作者：
Yangsheng Yu;K. Su
系统性红斑狼疮（SLE）是一种复杂的自身免疫性疾病，其特征是自身抗体的过量产生。SLE患者自身耐受性的丧失被认为是由先天和适应性免疫系统的失调引起的。中性粒细胞是先天免疫中最丰富的效应细胞，长期以来一直被证明与SLE有关。然而，它们在SLE发病机制中的作用尚不清楚，直到最近的研究发现SLE患者中性粒细胞胞外陷阱（NETs）的异常调节。网状结构是由染色质骨架和颗粒分子组成的网状结构。它们由活化的中性粒细胞通过“NETosis”过程释放出来。2004年，网络首次被描述为一种新的宿主防御机制，用于捕获和杀死外来病原体。最近的证据表明，NETs也参与多种炎症和自身免疫性疾病的发病机制，包括SLE。SLE患者NET的形成和清除之间的不平衡可能在自身免疫的持续和疾病的恶化以及终末器官表现的诱导中发挥重要作用。本文综述了目前关于NETs在SLE发病机制中的作用的研究结果。
Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by an overproduction of autoantibodies. The loss of self-tolerance in SLE is believed to be caused by the dysregulation of both innate and adaptive immune systems. Neutrophils, the most abundant effector cells of innate immunity, have long been shown to be associated with SLE. However, their role in the pathogenesis of SLE was not clear until recent studies discovered abnormal regulation of neutrophil extracellular traps (NETs) in SLE patients. NETs are web-like structures composed of chromatin backbones and granular molecules. They are released by activated neutrophils through a process called "NETosis". Nets were first described in 2004 as a novel host defense mechanism to trap and kill foreign pathogens. Recent evidence shows that NETs also participate in the pathogenesis of a variety of inflammatory and autoimmune diseases, including SLE. An imbalance between NET formation and clearance in SLE patients may play a prominent role in the perpetuation of autoimmunity and the exacerbation of disease, as well as the induction of end-organ manifestations. This review summarizes the current findings regarding the contribution of NETs to the pathogenesis of SLE.