Rheumatoid arthritis (RA) is a chronic and systemic autoimmune disease
with the decreasing proportion of regulatory T (Treg) cells. Previous
studies have shown that microRNAs (miRNAs, miR) act as key regulators of
Treg cells. In this study, we assessed the involvement of miR-143-3p on
Treg cells differentiation and function in the RA progress. We reported
that the expression of miR-143-3p has been negatively associated with RA
disease activity, and actively correlated with anti-inflammatory
cytokine IL-10, which was secreted by Treg cells. In vitro, miR-143-3p
expression in the CD4+T cells contributed to the upregulation of
forkhead box protein 3 (Foxp3), which was the characteristic
transcription factor of Treg cells. Notably, miR-143-3p mimics treatment
markedly upregulated the frequency of Treg cells in vivo, effectively
prevented CIA development and significantly inhibited inflammation in
mice. Altogether, we proposed that MiR-143-3p can alleviate CIA by
polarizing naive CD4+T cells into Treg cells, which warrants miR-143-3p
as a target for the new therapeutic strategy of Treg-deficiency
autoimmune diseases such as RA.
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