免疫学
补体系统
医学
系统性红斑狼疮
炎症
疾病
凝集素途径
自身免疫
促炎细胞因子
发病机制
补语(音乐)
自身免疫性疾病
替代补体途径
基因
免疫系统
抗体
生物
表型
遗传学
病理
互补
出处
期刊:Current Opinion in Rheumatology
[Ovid Technologies (Wolters Kluwer)]
日期:2002-09-01
卷期号:14 (5): 492-497
被引量:20
标识
DOI:10.1097/00002281-200209000-00002
摘要
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.
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