Abstract
Autoimmune diseases (AIDs) generally manifest as chronic immune disorders characterized by significant heterogeneity and complex symptoms. The discordant incidence of AIDs between monozygotic twins guided people to attach importance to environmental factors. Epigenetics is one of the major ways to be influenced, some of them can even occur years before clinical diagnosis. With the advent of high-throughput omics times, the mysterious veil of epigenetic modification in AIDs has been gradually unraveled, and some progress has been made in utilizing it as indicators of diagnosis and disease activity. For example, the hypomethylated IFI44L promoter in diagnosing systematic lupus erythematosus (SLE). More recently, newly identified noncoding RNAs (ncRNAs), including long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs), are also believed to be involved in the etiology of AIDs while the initial factor behind those epigenetic alterations can be diverse from metabolism to microbiota. Update and comprehensive insights into epigenetics in AIDs can help us understand the pathogenesis and further orchestrate it to benefit patients in the future. Therefore, we reviewed the latest epigenetic findings in SLE, rheumatoid arthritis (RA), Type 1 diabetes (T1D), systemic sclerosis (SSc) primarily from cellular levels.
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