Lewis Janet E, Fu Shu Man, Gaskin Felicia
Division of Rheumatology, Department of Medicine, University of Virginia School of Medicine, Charlottesville, Virginia 22908, USA.
Discov Med. 2013 Feb;15(81):85-92.
Systemic lupus erythematosus (SLE) is a prototype of systemic autoimmunity affecting many systems. Both antibodies and autoreactive T cells play significant roles in its pathogenesis. Experimental data and clinical observations indicate that autoimmunity and end organ damage are under separate genetic controls and that there are significant interactions between these two pathways. Experimental evidence has been obtained to support the hypothesis that autoantibodies and autoreactive T effector cells may be initiated by environmental factors through molecular mimicry and the inherent polyreactive nature of antigen receptors. A unified hypothesis has been postulated for the pathogenesis of SLE that has practical implications.
系统性红斑狼疮（SLE）是一种影响多个系统的系统性自身免疫病的典型例子。抗体和自身反应性T细胞在其发病机制中均起重要作用。实验数据和临床观察表明，自身免疫和终末器官损伤受不同的遗传控制，且这两条途径之间存在显著相互作用。已获得实验证据支持这样的假说，即自身抗体和自身反应性T效应细胞可能由环境因素通过分子模拟和抗原受体固有的多反应性引发。针对SLE的发病机制提出了一个具有实际意义的统一假说。
