Autoimmunity, end organ damage, and the origin of autoantibodies and autoreactive T cells in systemic lupus erythematosus.
Autoimmunity, end organ damage, and the origin of autoantibodies and autoreactive T cells in systemic lupus erythematosus.
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DOI：
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发表时间：
2013-02
影响因子：
1.4
通讯作者：
Janet E. Lewis;S. Fu;F. Gaskin
中科院分区：
文献类型：
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作者：
Janet E. Lewis;S. Fu;F. Gaskin
系统性红斑狼疮（SLE）是一种影响多系统的系统性自身免疫的原型。抗体和自身反应性T细胞在其发病机制中起重要作用。实验数据和临床观察表明，自身免疫和终末器官损伤是在不同的遗传控制下，这两个途径之间存在显着的相互作用。实验证据已经获得支持的假设，自身抗体和自身反应性T效应细胞可能通过分子模拟和抗原受体的固有多反应性的性质由环境因素启动。一个统一的假设已假定SLE的发病机制，具有实际意义。
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.