Molina Hector
Department of Medicine, Washington University School of Medicine, Saint Louis, Missouri 63110, USA.
Curr Opin Rheumatol. 2002 Sep;14(5):492-7. doi: 10.1097/00002281-200209000-00002.
Complement is involved in inflammation and in the optimization of adaptive responses. Abnormalities in the complement system have been associated with autoimmunity, especially systemic lupus erythematosus. A paradoxic relation exits between complement and lupus. Complement-mediated tissue damage is accepted as a mechanism in disease pathophysiology. Conversely, complement exerts a protective effect in disease development. The theoretic framework explaining this protective influence involves the adequate disposal of apoptotic material by classic pathway components. Inadequate clearance of apoptotic material may evoke a proinflammatory autoimmune response. This conceptual model is substantiated by studies indicating that complement receptor genes are within major susceptibility loci of systemic lupus erythematosus, that functional and structural abnormalities in these receptors are found in lupus mouse models, and that genetic polymorphism of lectin pathway genes correlates with increased risk of disease development. Finally, new diagnostic and therapeutic modalities based on complement regulation have been described in the past year.
补体参与炎症反应以及适应性免疫应答的优化。补体系统异常与自身免疫性疾病相关，尤其是系统性红斑狼疮。补体与狼疮之间存在一种矛盾的关系。补体介导的组织损伤被认为是疾病病理生理学中的一种机制。相反，补体在疾病发展过程中发挥保护作用。解释这种保护作用的理论框架涉及经典途径成分对凋亡物质的充分清除。凋亡物质清除不足可能引发促炎性自身免疫反应。表明补体受体基因位于系统性红斑狼疮的主要易感基因座内、在狼疮小鼠模型中发现这些受体存在功能和结构异常、凝集素途径基因的遗传多态性与疾病发展风险增加相关的研究证实了这一概念模型。最后，在过去一年中已经描述了基于补体调节的新诊断和治疗方法。
