Abstract
AbstractSystemic lupus erythematosus (SLE) is a common systemic autoimmune disease with complex aetiology, in which susceptibility is determined by the combination of genetic, environmental, epigenetic and stochastic factors. SLE is very heterogeneous in its clinical manifestations and the presence of different autoantibodies may predict different set of clinical outcome. However, despite considerable accumulated knowledge, the detailed pathogenesis of SLE still remains unknown. Several studies have indicated the importance ofdeoxyribonucleic acid(DNA) hypomethylation in the aetiology of SLE. Recent advances in high‐throughput genotyping technologies and high‐density genetic association studies have identified and replicated many SLE susceptibility genes in different populations. In this article, we outline our current understanding of some genetic and epigenetic aspects of SLE.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
