DNA methylation and autoirnmune disease
DNA methylation and autoirnmune disease
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DOI：
10.1016/s1521-6616(03)00206-7
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发表时间：
2003-10-01
影响因子：
8.6
通讯作者：
Richardson, B
中科院分区：
文献类型：
--
作者：
Richardson, B
DNA甲基化在维持T细胞功能方面发挥着至关重要的作用。越来越多的文献表明，未能维持成熟T细胞中的DNA甲基化水平和模式可导致体外T细胞自身反应性和体内自身免疫性。DNA甲基化的维持缺陷可能是由普鲁卡因胺或肼苯哒嗪等药物引起的，或者在有丝分裂期间未能激活编码维持DNA甲基转移酶的基因，导致狼疮样疾病或其他自身免疫性疾病的发展。本文综述了支持药物诱导狼疮动物模型中T细胞DNA甲基化异常在引起自身免疫中作用的证据，并讨论了一些相关机制。来自活动性狼疮患者的T细胞有证据表明大多数（如果不是全部）相同的甲基化异常，这表明异常的DNA甲基化在特发性人类狼疮中也起作用。(C)2003年爱思唯尔公司All rights reserved.
DNA methylation plays an essential role in maintaining T-cell function. A growing body of literature indicates that failure to maintain DNA methylation levels and patterns in mature T cells can result in T-cell autoreactivity in vitro and autoimmunity in vivo. Defective maintenance of DNA methylation may be caused by drugs such as procainamide or hydralazine, or failure to activate the genes encoding maintenance DNA methyltransferases during mitosis, resulting in the development of a lupus-like disease or perhaps other autoimmune disorders. This paper reviews the evidence supporting a role for abnormal T-cell DNA methylation in causing autoimmunity in an animal model of drug-induced lupus, and discusses some of the mechanisms involved. T cells from patients with active lupus have evidence for most if not all of the same methylation abnormalities, suggesting that abnormal DNA methylation plays a role in idiopathic human lupus as well. (C) 2003 Elsevier Inc. All rights reserved.