Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 128, Issue 6, Pages 2551-2568Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI97426
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Funding
- National Science Fund for Excellent Young Scholars [81522038]
- Project of Innovation-driven Plan of Central South University [2016CX029]
- National Natural Science Foundation of China [81371743, 81573051]
- Key Program of National Natural Science Foundation of China [81430074]
- Fundamental Research Funds for the Central Universities of Central South University [2016zzts143]
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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 arid 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 TGP-beta and IL-23 enhance miR-210 expression by inducing HIF-1 alpha, 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.
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