As is discussed previously, environmental factors and epigenetic dysregulation are the important pathogenic factors in the development of this autoimmune disease. Beside DNA methylation abnormalities, changes in histones and noncoding RNAs are also suggested to be involved in the process.
Previous studies have indicated that global hypoacetylation of the histones H3 and H4 in CD4+ T cells from SLE patients shows a negative correlation between the level of H3 histone acetylation and disease. Moreover, in a mouse SLE model, trichostatin A (TSA), the HDAC inhibitor, has been found to restore a normal level of histone acetylation and improve the clinical manifestations of SLE.
Several miRNAs also have been implicated in the pathogenesis of autoimmune disease systemic lupus erythematosus (SLE). For example, peripheral blood mononuclear cells from SLE patients shows increased levels in some miRNAs (such as miR-189, miR-61, miR-78, miR-21, miR-142-3p, miR-342, miR-299-3p, miR-198, and miR-298) and decreased levels in others (such as miR-196a, miR-17-5p, miR-409-3p, miR-141, miR-383, miR-112, and miR-184).
Once dysregulation of epigenome is found in SLE patients versus controls, according to these regulatory mechanisms, the expression and function of related emzymes may be used as therapeutic targets or tools in SLE.