| Literature DB >> 28774595 |
Ziwei Jiang1, Yuanqi Liu1, Changwei Li1, Leilei Chang1, Wang Wang1, Zhenhua Wang1, Xiaoguang Gao1, Bernhard Ryffel2, Yelin Wu1, Yuping Lai3.
Abstract
IL-36 family members are highly expressed in hyperproliferative keratinocytes and play an important role in the pathogenesis of skin diseases such as psoriasis. However, whether and how IL-36 cytokines are induced to promote wound healing remains unknown. Here we showed that skin injury increased the expression of IL-36γ to promote wound healing. Mechanistically, the expression of IL-36γ was induced by RNAs from damaged cells via the activation of toll-like receptor 3 (TLR3) and TIR-domain-containing adapter-inducing IFN-β (TRIF) followed by the induction of a zinc finger protein SLUG to abrogate the inhibitory effect of vitamin D receptor (VDR) on the promoter of IL-36γ gene. IL-36γ acted back on keratinocytes to induce REG3A, which regulated keratinocyte proliferation and differentiation, thus promoting wound re-epithelialization. These observations show that skin injury increases IL-36γ via the activation of TLR3-SLUG-VDR axis and that IL-36γ induces REG3A to promote wound healing. These findings also provide insights into pathways contributing to wound repair.Entities:
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Year: 2017 PMID： 28774595 DOI： 10.1016/j.jid.2017.07.820
Source DB: PubMed Journal: J Invest Dermatol ISSN： 0022-202X Impact factor: 8.551