转录因子Ets1在狼疮及其他自身免疫性疾病中的作用
The Role of the Transcription Factor Ets1 in Lupus and Other Autoimmune Diseases.
作者信息
Garrett-Sinha Lee Ann, Kearly Alyssa, Satterthwaite Anne B
机构信息
Department of Biochemistry, State University of New York at Buffalo, Buffalo, NY 14203.
Department of Internal Medicine, Rheumatic Diseases Division; Department of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390.
出版信息
Crit Rev Immunol. 2016;36(6):485-510. doi: 10.1615/CritRevImmunol.2017020284.
Abstract
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by excess B- and T-cell activation, the development of autoantibodies against self-antigens including nuclear antigens, and immune complex deposition in target organs, which triggers an inflammatory response and tissue damage. The genetic and environmental factors that contribute to the development of SLE have been studied extensively in both humans and mouse models of the disease. One of the important genetic contributions to SLE development is an alteration in the expression of the transcription factor Ets1, which regulates the functional differentiation of lymphocytes. Here, we review the genetic, biochemical, and immunological studies that have linked low levels of Ets1 to aberrant lymphocyte differentiation and to the pathogenesis of SLE.
摘要
系统性红斑狼疮（SLE）是一种慢性自身免疫性疾病，其特征在于B细胞和T细胞过度活化、针对包括核抗原在内的自身抗原产生自身抗体，以及免疫复合物在靶器官中沉积，从而引发炎症反应和组织损伤。在人类和该疾病的小鼠模型中，对导致SLE发生的遗传和环境因素进行了广泛研究。对SLE发生的重要遗传贡献之一是转录因子Ets1表达的改变，该因子调节淋巴细胞的功能分化。在此，我们综述了将低水平Ets1与异常淋巴细胞分化及SLE发病机制联系起来的遗传、生化和免疫学研究。
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