| First Author | Tanno H | Year | 2015 |
| Journal | Am J Pathol | Volume | 185 |
| Issue | 12 | Pages | 3248-57 |
| PubMed ID | 26468976 | Mgi Jnum | J:227764 |
| Mgi Id | MGI:5702784 | Doi | 10.1016/j.ajpath.2015.08.012 |
| Citation | Tanno H, et al. (2015) Contribution of Invariant Natural Killer T Cells to Skin Wound Healing. Am J Pathol 185(12):3248-57 |
| abstractText | In the present study, we determined the contribution of invariant natural killer T (iNKT) cells to the skin wound healing process. In iNKT cell-deficient (Jalpha18KO) mice lacking iNKT cells, wound closure was significantly delayed compared with wild-type mice. Collagen deposition, expression of alpha-smooth muscle actin and CD31, and wound breaking strength were significantly attenuated in Jalpha18KO mice. The adoptive transfer of liver mononuclear cells from wild-type but not from Jalpha18KO or interferon (IFN)-gamma gene-disrupted (IFN-gammaKO) mice resulted in the reversal of this impaired wound healing in Jalpha18KO mice. IFN-gamma expression was induced in the wounded tissues, which was significantly decreased at 6, 12, and 24 hours, but increased on day 3 after wounding in Jalpha18KO mice. The main source of the late-phase IFN-gamma production in Jalpha18KO mice were neutrophils rather than NK cells and T cells. Administration of alpha-galactosylceramide, an activator of iNKT cells, resulted in the acceleration of wound healing on day 3 in wild-type mice. This effect was not observed in IFN-gammaKO mice. These results indicate that iNKT cells play important roles in wound healing. The iNKT cell-induced IFN-gamma production may regulate the wound healing process in the early phase. |
