More recently, it has become clear that epigenetic factors play a key role in the immune pathogenesis of SLE [10–12]. Methylation of CpG (meCpG) DNA motifs, post-transcriptional modifications to histone tails, and micro-RNA (miRNA)-mediated effects alter nucleosome conformations, eventually affecting gene expression and subsequent cellular processes. UV radiation, drug exposure, and viral infections have all been documented to influence meCpG patterns in T and B cells because they trigger important interactions between environment and host [13]. In general, SLE is associated with (global) CpG hypomethylation in B and T lymphocytes [14,15]. Histone modifications in immune cells from SLE patients are complex and display patterns that are tissue- and cell type-specific. Epigenetic alterations in SLE patients have been attributed to the abundance and/or activity of DNA methyltransferases (DNMTs) and histone deacetylases (HDACs) [10]. Through their effects on chromatin conformation, DNMTs and HDACs modify DNA accessibility, controlling access by transcription factors and RNA polymerases, and thereby regulating gene expression [10]. However, the precise mechanisms by which these enzymes are specifically recruited to genes in immune cells from SLE patients remain poorly understood.
