Liu Chau-Ching, Navratil Jeannine S, Sabatine Janice M, Ahearn Joseph M
Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Pittsburgh School of Medicine, Lupus Center of Excellence, University of Pittsburgh Schools of the Health Sciences, Pittsburgh, Pa., USA.
Curr Dir Autoimmun. 2004;7:49-86. doi: 10.1159/000075687.
Deficiencies in the classical pathway of the complement system have been implicated in the etiology and pathogenesis of systemic lupus erythematosus (SLE) for several decades. Recent advances have suggested that this link is due to a critical role of complement in the recognition and clearance of the cellular remnants of apoptosis. In this review, we summarize the role of apoptosis in generation of an autoimmune response, and we integrate recent advances that link apoptosis, complement activation and the etiopathogenesis of SLE.
几十年来，补体系统经典途径的缺陷一直被认为与系统性红斑狼疮（SLE）的病因和发病机制有关。最近的研究进展表明，这种联系是由于补体在细胞凋亡残余物的识别和清除中起关键作用。在这篇综述中，我们总结了细胞凋亡在自身免疫反应产生中的作用，并整合了将细胞凋亡、补体激活与SLE的病因发病机制联系起来的最新进展。
