No abstract

T helper 17 (Th17) cells have a pathogenic effect in many autoimmune diseases. Inhibition of Th17 cells can alleviate the inflammatory damage in autoimmune diseases. Our previous study found that microRNA‐590‐3p (miR‐590‐3p) was involved in the differentiation of Th17 cells in systemic lupus erythematosus (SLE). Here, we demonstrated that an increase in Th17 cells was correlated with low expression of miR‐590‐3p in patients with SLE and in lupus mice. Upregulation of miR‐590‐3p reduced the differentiation and promoted apoptosis of Th17 cells. Subsequent experiments demonstrated that miR‐590‐3p promoted apoptosis in Th17 cells by inhibiting autophagy. Autophagy‐related 7 (Atg7) was the direct target of miR‐590‐3p that blocked the autophagy pathway. Finally, treatment of MRL/lpr mice with miR‐590‐3p agomir ameliorated lupus nephritis and skin lesions. Our work revealed that miR‐590‐3p inhibited Th17 cells by suppressing autophagy and that increased miR‐590‐3p expression was able to ameliorate the clinical symptoms of lupus. Therefore, miR‐590‐3p may be a promising therapeutic target for SLE and other Th17 cell‐dependent autoimmune diseases.

T helper 17 (Th17) cells are characterized by the secretion of the IL-17 cytokine and are essential for the immune response against bacterial and fungal infections. Despite the beneficial roles of Th17 cells, unrestrained IL-17 production can contribute to immunopathology and inflammatory autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, and inflammatory bowel disease. Although these diverse outcomes are directed by the activation of Th17 cells, the regulation of Th17 cells is incompletely understood. The discovery that microRNAs (miRNAs) are involved in the regulation of Th17 cell differentiation and function has greatly improved our understanding of Th17 cells in immune response and disease. Here, we provide an overview of the biogenesis and function of miRNA and summarize the role of miRNAs in Th17 cell differentiation and function. Finally, we focus on recent advances in miRNA-mediated dysregulation of Th17 cell fate in autoimmune diseases.