Epigenetics of Psoriasis

Psoriasis is a chronic and recurrent inflammatory skin disease, involving the rapid proliferation and abnormal differentiation of keratinocytes and activation of T cells. It is generally accepted that the central pathogenesis of psoriasis is a T cell-dominant immune disorder affected by multiple factors including genetic susceptibility, environmental factors, innate and adaptive immune responses, etc. However, the exact etiology is largely unknown. In recent years, epigenetic involvements, such as the DNA methylation, chromatin modifications, and noncoding RNA regulation are reported to be critical for the pathogenesis of psoriasis. However, the interplay between these factors has only recently been started to be unraveled. Notably, inhibitors of enzymes that work in epigenetic modifications, such as DNA methyltransferases and histone deacetylases, are beginning to appear in the clinical setting to restore normal epigenetic patterns (Generali et al. in J Autoimmun 83:51–61, 2017), providing novel therapeutic potential as novel treatment targets for psoriasis. Indeed, medications previously used to treat autoimmune diseases have later been discovered to exert their action via epigenetic mechanisms. Herein, we review the findings on epigenetics associated with psoriasis, and discuss future perspectives in this field.