Cytokines and miRNAs in the Pathogenesis of Rheumatoid Arthritis: A Review
Rheumatoid Arthritis (RA) is a chronic autoimmune disease characterized by inflammatory synovial hyperplasia. The pathogenesis of RA may be related to heredity, infection and sex hormones. The initial stage of RA involves the activation of T cells. Immature CD4+ T cells differentiate into T helper (Th) cells and T regulatory (Treg) cells under antigen stimulation and cytokine signal transduction. Cytokines secreted by Th cells and Treg cells play crucial roles in the pathophysiology of RA. The cytokines can be roughly divided into proinflammatory cytokines, anti-inflammatory cytokines, and both pro- and antiinflammatory cytokines. The imbalance between pro-inflammatory cytokines and anti-inflammatory cytokines would lead to a variety of autoimmune diseases. The disease severity was significantly indicated by serum or plasma cytokine levels with RA patients. Many clinical trials have shown that anticytokine drugs are effective in treating RA. This article reviews the differentiation process of different Th cells and Treg cells, the roles of cytokines secreted by them in the pathogenesis of RA and how miRNAs mediate immune regulation in RA. By understanding the roles of cytokines and miRNAs in the pathogenesis of autoimmunity, it is necessary to develop potential anti-cytokine drugs and biomarkers/therapeutic targeted drugs through various ways in the treatment of RA.