Abstract
Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease in which the body’s immune system mistakenly attacks healthy cells. Although the exact cause of SLE has not been identified, it is clear that both genetics and environmental factors trigger the disease. Identical twins have a 24% chance of getting lupus disease if the other one is affected. Internal factors such as female gender and sex hormones, the major histocompatibility complex (MHC) locus and other genetic polymorphisms have been shown to affect SLE, as well as external, environmental influences such as sunlight exposure, smoking, vitamin D deficiency, and certain infections. Several studies have reported and proposed multiple associations between the alteration of the epigenome and the pathogenesis of autoimmune disease. Epigenetic factors contributing to SLE include microRNAs, DNA methylation status, and the acetylation/deacetylation of histone proteins. Additionally, the acetylation of non-histone proteins can also influence cellular function. A better understanding of non-genomic factors that regulate SLE will provide insight into the mechanisms that initiate and facilitate disease and also contribute to the development of novel therapeutics that can specifically target pathogenic molecular pathways.
Highlights
Systemic lupus erythematosus (SLE) is a pathophysiologically complex systemic autoimmune disease affecting multiple organs [1,2,3]
Our studies have demonstrated that histone deacetylases (HDACs) are significantly upregulated in lymphocytes in MRL/lpr lupus prone mice [9,10]
In New Zealand Black/White (NZB/W) F1 female mice, trichostatin A (TSA) administration resulted in an increase in regulatory T cells and a decrease of CD69+ activated T helper cells which correlated with reduced lupus nephritis [111]
Summary
Systemic lupus erythematosus (SLE) is a pathophysiologically complex systemic autoimmune disease affecting multiple organs [1,2,3]. Epigenetic regulation may involve microRNAs, acetylation and methylation of histone proteins and DNA methylation—all of which have been linked to the initiation, onset, progression and perpetuation of SLE [6,7,8]. Other studies have found elevated histone acetylation in innate immune cells, such as monocytes [11,12,13]. Studies have shown that global alteration of DNA methylation is pathogenic in lymphocytes and innate immune cells; hypomethylation has been highly correlated with disease activities in SLE patients [14]. We will briefly summarize the role of DNA methylation in SLE and highlight immunopathogenic contributions of acetylation and deacetylation to lupus
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