Systemic lupus erythematosus (SLE) is a prototypical autoimmune disease 
characterized by production of autoantibodies against a series of nuclear 
antigens. Although the exact cause of SLE is still unknown, the influence of 
environment, which is largely reflected by the epigenetic mechanisms, with DNA 
methylation changes in particular, are generally considered as key players in 
the pathogenesis of SLE. As an important post-translational modification, DNA 
methylation mainly suppresses the expression of relevant genes. Accumulating 
evidence has indicated that abnormal DNA hypomethylation in T cells is an 
important epigenetic hallmark in SLE. Apart from those classic 
methylation-sensitive autoimmunity-related genes in lupus, such as CD11a 
(ITGAL), Perforin (PRF1), CD70 (TNFSF7), CD40 ligand (TNFSF5) and PP2Acα, the 
genome-wide methylation pattern has also been explored recently, providing us a 
more and more full-scale picture of the abnormal status of DNA methylation in 
SLE. On the other hand, certain miRNAs, RFX1, defective ERK pathway signaling, 
Gadd45α and DNA hydroxymethylation have been proposed as potential mechanisms 
leading to DNA hypomethylation in lupus. In this review, we summarize current 
understanding of T cell DNA methylation changes and the consequently altered 
gene expressions in lupus, and how they contribute to the development of SLE. 
Possible mechanisms underlying these aberrancies are also discussed based on the 
reported literature and our own findings.