| First Author | Jiang Z | Year | 2017 |
| Journal | J Invest Dermatol | Volume | 137 |
| Issue | 12 | Pages | 2620-2629 |
| PubMed ID | 28774595 | Mgi Jnum | J:296063 |
| Mgi Id | MGI:6467017 | Doi | 10.1016/j.jid.2017.07.820 |
| Citation | Jiang Z, et al. (2017) IL-36gamma Induced by the TLR3-SLUG-VDR Axis Promotes Wound Healing via REG3A. J Invest Dermatol 137(12):2620-2629 |
| abstractText | 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-36gamma to promote wound healing. Mechanistically, the expression of IL-36gamma was induced by RNAs from damaged cells via the activation of toll-like receptor 3 (TLR3) and TIR-domain-containing adapter-inducing IFN-beta (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-36gamma gene. IL-36gamma 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-36gamma via the activation of TLR3-SLUG-VDR axis and that IL-36gamma induces REG3A to promote wound healing. These findings also provide insights into pathways contributing to wound repair. |
