Journal
CLINICAL SCIENCE
Volume 134, Issue 16, Pages 2209-2222Publisher
PORTLAND PRESS LTD
DOI: 10.1042/CS20200799
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Funding
- NSFC [81671592]
- Science and Technology Department of Jilin Province [20180101110JC, 20190201140JC]
- Finance Department of Jilin Province [JLSWSRCZX2020-089]
- Education Department of Jilin Province [JJKH20201064KJ]
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Immune cells play important roles in systemic lupus erythematosus (SLE). We previously a found that myeloid-derived suppressor cell (MDSC)-derived arginase-1 (Arg-1) promoted Th17 cell differentiation in SLE. In the present study, we performed RNA-chip to identify the microRNA regulation network between MDSCs and Th17 cells. miR-542-5p in humans, as the homologous gene of miR-322-5p in mice was significantly up-regulated in the Th17+MDSC group compared with Th17 cells cultured alone and down-regulated in the Th17+MDSC+Arg-1 inhibitor group compared with the Th17+MDSC group. We further evaluated the miR-322-5p and Th17/Treg balance in mice and found that the proportions of both Th17 cells and Tregs were elevated and that miR-322-5p overexpression activated the transforming growth factor-beta pathway. Moreover, although miR-322-5p expression was higher in SLE mice, it decreased after treatment with an Arg-1 inhibitor. The proportion of Th17 cells and Th17/Treg ratio correlated with miR-322-5p levels. In conclusion, MDSC-derived Arg-1 and mmu-miR-322-5p not only promote Th17 cell and Treg differentiation, but also shift the Th17/Treg ratio in SLE. The Arg-1/miR-322-5p axis may serve as a novel treatment target for SLE.
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