MicroRNA‐mediated regulation of T helper type 17/regulatory T‐cell balance in autoimmune disease

Summary T helper type 17 (Th17) cells and regulatory T (Treg) cells are two distinct T‐cell subsets with opposite effects on immune functions. While Th17 cells are a key effector in the immune response and play critical roles in the development of autoimmunity and inflammation, Treg cells orchestrate the overall immune response and maintain peripheral immune tolerance by regulating the activity of the effector T cells. However, the developmental pathways for Th17 and Treg cells are reciprocally interconnected and there is a significant amount of plasticity between them. Disturbed Th17/Treg balance contributes to the development of autoimmune diseases, like experimental autoimmune encephalomyelitis and multiple sclerosis. MicroRNAs (miRNAs) are small non‐coding RNA molecules that post‐transcriptionally regulate gene expression. Recently, emerging evidence demonstrates that miRNAs play an important role in regulating the pathogenesis of autoimmune diseases through the modulation of Th17/Treg balance. This review will provide an overview of the dysregulated miRNAs and their functions in modulating the Th17/Treg balance in autoimmune diseases. Th17/Treg balance is critical for immune homeostasis and its dysregulation leads to autoimmune disease. MicroRNAs are small non‐coding RNA molecules that post‐transcriptionally regulate gene expression. Emerging evidence demonstrates that microRNAs play an important role in modulating Th17/Treg balance.