The Role of the Transcription Factor Ets1 in Lupus and Other Autoimmune Diseases.
The Role of the Transcription Factor Ets1 in Lupus and Other Autoimmune Diseases.
复制标题
DOI：
10.1615/critrevimmunol.2017020284
复制
发表时间：
2016
影响因子：
1.3
通讯作者：
Satterthwaite AB
中科院分区：
文献类型：
--
作者：
Garrett-Sinha LA;Kearly A;Satterthwaite AB
系统性红斑狼疮（SLE）是一种慢性自身免疫性疾病，其特征在于过量的B和T细胞活化，针对自身抗原（包括核抗原）的自身抗体的产生，以及免疫复合物在靶器官中的沉积，其触发炎症反应和组织损伤。促进SLE发展的遗传和环境因素已在人类和小鼠疾病模型中进行了广泛研究。SLE发展的重要遗传贡献之一是调节淋巴细胞功能分化的转录因子Ets1表达的改变。在这里，我们回顾了遗传学，生物化学和免疫学的研究表明，低水平的Ets1异常淋巴细胞分化和SLE的发病机制。
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 development of SLE have been extensively studied 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.