Contribution of invariant natural killer T cells to skin wound healing

Hiromasa Tanno, Kazuyoshi Kawakami, Masae Ritsu, Emi Kanno, Aiko Suzuki, Rina Kamimatsuno, Naoyuki Takagi, Tomomitsu Miyasaka, Keiko Ishii, Yoshimichi Imai, Ryoko Maruyama, Masahiro Tachi

Research output: Contribution to journalArticlepeer-review

29 Citations (Scopus)


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 (Jα18KO) mice lacking iNKT cells, wound closure was significantly delayed compared with wild-type mice. Collagen deposition, expression of α-smooth muscle actin and CD31, and wound breaking strength were significantly attenuated in Jα18KO mice. The adoptive transfer of liver mononuclear cells from wild-type but not from Jα18KO or interferon (IFN)-γ gene-disrupted (IFN-γKO) mice resulted in the reversal of this impaired wound healing in Jα18KO mice. IFN-γ 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 Jα18KO mice. The main source of the late-phase IFN-γ production in Jα18KO mice were neutrophils rather than NK cells and T cells. Administration of α-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-γKO mice. These results indicate that iNKT cells play important roles in wound healing. The iNKT cell-induced IFN-γ production may regulate the wound healing process in the early phase.

Original languageEnglish
Pages (from-to)3248-3257
Number of pages10
JournalAmerican Journal of Pathology
Issue number12
Publication statusPublished - 2015 Dec


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