The role of epigenetic variation in the pathogenesis of systemic lupus erythematosus
1 Arthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA
2 Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA
3 US Department of Veterans Affairs Medical Center, Oklahoma City, OK 73104, USA
4 825 NE 13th Street, MS#24, Oklahoma City, OK 73104, USA
Citation and License
Arthritis Research & Therapy 2011, 13:245 doi:10.1186/ar3484Published: 31 October 2011
The focus of the present review is on the extent to which epigenetic alterations influence the development of systemic lupus erythematosus. Lupus is a systemic autoimmune disease characterized by the production of autoantibodies directed at nuclear self-antigens. A DNA methylation defect in CD4+ T cells has long been observed in idiopathic and drug-induced lupus. Recent studies utilizing high-throughput technologies have further characterized the nature of the DNA methylation defect in lupus CD4+ T cells. Emerging evidence in the literature is revealing an increasingly interconnected network of epigenetic dysregulation in lupus. Recent reports describe variable expression of a number of regulatory microRNAs in lupus CD4+ T cells, some of which govern the expression of DNA methyltransferase 1. While studies to date have revealed a significant role for epigenetic defects in the pathogenesis of lupus, the causal nature of epigenetic variation in lupus remains elusive. Future longitudinal epigenetic studies in lupus are therefore needed.