文献类型：期刊文献

英文题名：Autoimmunity, End Organ Damage, and the Origin of Autoantibodies and Autoreactive T Cells in Systemic Lupus Erythematosus

作者：Lewis, Janet E.[1];Fu, Shu Man[2,3,4];Gaskin, Felicia[5]

机构：[1]Univ Virginia, Sch Med, Dept Med, Div Rheumatol, Charlottesville, VA 22908 USA;[2]Univ Virginia, Sch Med, Dept Med, Charlottesville, VA 22908 USA;[3]Univ Virginia, Sch Med, Dept Microbiol Immunol & Canc Biol, Charlottesville, VA 22908 USA;[4]Univ Virginia, Sch Med, CIIR, Charlottesville, VA 22908 USA;[5]Univ Virginia, Sch Med, Dept Psychiat & Neurobehav Sci, Charlottesville, VA 22908 USA

年份：2013

卷号：15

期号：81

起止页码：85

外文期刊名：DISCOVERY MEDICINE

收录：SCI-EXPANDED(收录号：WOS:000316992500002)、、WOS

基金：We thank Ms. Lena Garrison for her help in preparing this manuscript. This work was supported in part by NIH grants P50-AR04522, R01-AR047988, R01-AR049449, and R01-AI079621 and grants from Alliance for Lupus Research.

语种：英文

外文摘要：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. [Discovery Medicine 15(81):85-92, February 2013]