Karp David R
Rheumatic Diseases Division, The University of Texas Southwestern Medical Center at Dallas, 75390, USA.
Curr Opin Rheumatol. 2005 Sep;17(5):538-42. doi: 10.1097/01.bor.0000172799.03379.86.
It is well recognized that the complement system plays multiple roles in systemic lupus erythematosus. Activation of the classical pathway by immune complexes leads to the generation of inflammatory mediators, thus promoting tissue injury. Complement activation also plays an important role in the maintenance of tolerance to self-antigens. This review discusses recent insights in the role of complement in the pathogenesis of systemic lupus erythematosus.
The antiphospholipid syndrome is a major feature of systemic lupus erythematosus. New findings have clearly demonstrated that the prothrombotic effects seen in a mouse model of this syndrome depend on complement activation, whereas the protective effects of heparin are due to its anticomplementary effects rather than its anticoagulant action. Secondly, a potential mechanism explaining the association of anti-C1q autoantibodies with lupus glomerulonephritis has been elucidated in a mouse model system.
New findings have helped to reinforce the role of complement in the etiology and tissue damage of systemic lupus erythematosus. These findings point to more precise, mechanism-based therapies for autoimmune and inflammatory disease.
补体系统在系统性红斑狼疮中发挥多种作用已得到广泛认可。免疫复合物激活经典途径会导致炎症介质的产生，从而促进组织损伤。补体激活在维持对自身抗原的耐受性方面也起着重要作用。本综述讨论了补体在系统性红斑狼疮发病机制中作用的最新见解。
抗磷脂综合征是系统性红斑狼疮的一个主要特征。新发现清楚地表明，在该综合征小鼠模型中观察到的促血栓形成作用取决于补体激活，而肝素的保护作用是由于其抗补体作用而非抗凝作用。其次，在小鼠模型系统中阐明了一种解释抗C1q自身抗体与狼疮性肾炎关联的潜在机制。
新发现有助于强化补体在系统性红斑狼疮病因和组织损伤中的作用。这些发现指向针对自身免疫性和炎症性疾病更精确、基于机制的治疗方法。
