MicroRNA‐590‐3p inhibits T helper 17 cells and ameliorates inflammation in lupus mice.

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. [ABSTRACT FROM AUTHOR]

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