| First Author | Wu R | Year | 2018 |
| Journal | J Clin Invest | Volume | 128 |
| Issue | 6 | Pages | 2551-2568 |
| PubMed ID | 29757188 | Mgi Jnum | J:277878 |
| Mgi Id | MGI:6162221 | Doi | 10.1172/JCI97426 |
| Citation | Wu R, et al. (2018) MicroRNA-210 overexpression promotes psoriasis-like inflammation by inducing Th1 and Th17 cell differentiation. J Clin Invest 128(6):2551-2568 |
| abstractText | Immune imbalance of T lymphocyte subsets is a hallmark of psoriasis, but the molecular mechanisms underlying this aspect of psoriasis pathology are poorly understood. Here, we report that microRNA-210 (miR-210), a miR that is highly expressed in both psoriasis patients and mouse models, induces helper T (Th) 17 and Th1 cell differentiation but inhibits Th2 differentiation through repressing STAT6 and LYN expression, contributing to several aspects of the immune imbalance in psoriasis. Both miR-210 ablation in mice and inhibition of miR-210 by intradermal injection of antagomir-210 blocked the immune imbalance and the development of psoriasis-like inflammation in an imiquimod-induced or IL-23-induced psoriasis-like mouse model. We further showed that TGF-beta and IL-23 enhance miR-210 expression by inducing HIF-1alpha, which recruits P300 and promotes histone H3 acetylation in the miR-210 promoter region. Our results reveal a crucial role for miR-210 in the immune imbalance of T lymphocyte subsets in psoriasis and suggest a potential therapeutic avenue. |
