MicroRNA-10b promotes arthritis development by disrupting CD4+ T cell subtypes

Rheumatoid arthritis (RA) is an inflammation-involved disorder and features the disruption of CD4(+) T lymphocytes. Herein, we describe that microRNA-10b-5p (miR-10b) promotes RA progression by disrupting the balance between subsets of CD4(+) T cells. MiR-10b-deficient mice protected against collagen antibody-induced arthritis (CAIA) model. RNA sequencing results indicated that disordered genes in miR-10b(-/-) CAIA model are closely associated with CD4(+) T cells differentiation. Moreover, miR-10b mimics promoted Th1/Th17 and suppressed Th2/Treg cells differentiation, whereas miR-10b inhibitor induced contrary effects. In addition, GATA3 and PTEN was confirmed as two targets of miR-10b, and GATA3 siRNA could increase Th1 and reduce Th2 cells meanwhile PTEN siRNA could increase Th17 and decrease Treg cells. Furthermore, miR-10b inhibitor significantly ameliorated collagen-induced arthritis (CIA) development by attenuating the dysfunctional CD4(+) T cell subpopulations. The present findings suggest that miR-10b could disrupt the balance of CD4(+) T subsets, while suppressed miR-10b could attenuate the severity of experimental arthritis, which provided us a novel mechanistic and therapeutic insight into the RA.

Automated summary

miR-10b disrupts the balance of CD4(+) T cell subsets and promotes the progression of rheumatoid arthritis (RA). Inhibiting miR-10b can alleviate the severity of arthritis.