Linking complement and anti-dsDNA antibodies in the pathogenesis of systemic lupus erythematosus.
Linking complement and anti-dsDNA antibodies in the pathogenesis of systemic lupus erythematosus.
复制标题
在全身性红斑狼疮的发病机理中连接补体和抗DSDNA抗体。
DOI：
10.1007/s12026-012-8345-z
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发表时间：
2013-03
影响因子：
4.4
通讯作者：
Boackle SA
中科院分区：
文献类型：
--
作者：
Giles BM;Boackle SA
系统性红斑狼疮是一种严重的自身免疫性疾病，会影响多个器官系统，导致不同的症状和结果。其特点是产生针对多种自身抗原的抗体，但它与抗 dsDNA 抗体特异性相关。抗 dsDNA 抗体在临床疾病发作之前就存在，并且与狼疮的严重表现（例如肾小球肾炎）相关。它们的水平随着疾病活动度的变化而波动，与补体蛋白 C3 和 C4 的水平相结合，是狼疮患者疾病发作和治疗反应的有力指标。狼疮活动期间注意到的补体水平下降被认为是继发于自身抗体产生和免疫复合物形成增加，从而导致组织损伤；然而，最近的数据表明，补体激活也可以驱动这些致病性自身抗体的发展。本综述将探讨补体在抗 dsDNA 抗体的发育和发病机制中的各种作用。
Systemic lupus erythematosus is a severe autoimmune disease that affects multiple organ systems resulting in diverse symptoms and outcomes. It is characterized by antibody production to a variety of self-antigens, but it is specifically associated with those against anti-dsDNA. Anti-dsDNA antibodies are present before the onset of clinical disease and are associated with severe manifestations of lupus such as glomerulonephritis. Their levels fluctuate with changes in disease activity and, in combination with the levels of complement proteins C3 and C4, are strong indicators of disease flare and treatment response in patients with lupus. The decreased complement levels that are noted during flares of lupus activity are believed to be secondary to increased autoantibody production and immune complex formation that results in tissue damage; however, recent data suggest that complement activation can also drive development of these pathogenic autoantibodies. This review will explore the various roles of complement in the development and pathogenesis of anti-dsDNA antibodies.
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