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.

Automated summary

Inhibition of T helper 17 cells through upregulation of miR-590-3p reduces inflammation in autoimmune diseases like SLE. Our study shows that miR-590-3p promotes apoptosis in Th17 cells by inhibiting autophagy, offering a promising therapeutic strategy for SLE.