The Pathogenic Role of Dysregulated Epigenetic Modifications in Autoimmune Diseases

Autoimmune diseases can be chronic with relapse of inflammatory symptoms, but it can be also acute and life-threatening if immune cells destroy life-supporting organs, such as lupus nephritis. The etiopathogenesis of autoimmune diseases has been revealed as that genetics and environmental factors-mediated dysregulated immune responses contribute to the initiation and development of autoimmune disorders. However, the current understanding of pathogenesis is limited and the underlying mechanism has not been well defined, which lows the development of novel biomarkers and new therapeutic strategies for autoimmune diseases. To improve this, broadening and deepening our understanding of pathogenesis is an unmet need. As genetic susceptibility cannot explain the low accordance rate of incidence in homozygous twins, epigenetic regulations might be an additional explanation. Therefore, this review will summarize current progress of studies on epigenetic dysregulations contributing to autoimmune diseases, including SLE, rheumatoid arthritis (RA), psoriasis, type 1 diabetes (T1D), and systemic sclerosis (SSc), hopefully providing opinions on orientation of future research, as well as discussing the clinical utilization of potential biomarkers and therapeutic strategies for these diseases.