A novel role for NKT cells in cutaneous wound repair.
Here, we report the novel observation that natural killer T (NKT) cells contribute to the cutaneous wound repair process. Using an excisional wound model in wild-type versus NKT cell-deficient mice, this report shows that when NKT cells are absent, initial wound closure is markedly accelerated. We report here for the first time that NKT cells are a significant constituent of early wound inflammation and that they regulate the local production of a key subset of neutrophil and monocyte/macrophage chemokines, as well as TGF-β1 content and collagen deposition. Together, our findings support the concept that NKT cells regulate the early inflammatory and fibroproliferative phases of nonpathologic healing wounds, positioning the NKT cell as an attractive potential therapeutic target for modulation of impaired wound healing.
Schneider
David F
DF
The Department of Surgery, Burn and Shock Trauma Institute, Maywood, Illinois, USA.
Palmer
Jessica L
JL
Tulley
Julia M
JM
Speicher
John T
JT
Kovacs
Elizabeth J
EJ
Gamelli
Richard L
RL
Faunce
Douglas E
DE
D000818:Animals; D055610:Antigens, CD1d; D018925:Chemokines / Q000378:metabolism; D003094:Collagen / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D018345:Mice, Knockout; D055611:Natural Killer T-Cells / Q000502:physiology*; D020556:Neutrophil Infiltration; D010586:Phagocytes / Q000502:physiology; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D014945:Wound Healing / Q000276:immunology*
D055610:Antigens, CD1d; D018925:Chemokines; C508961:Tgfb1 protein, mouse; D053773:Transforming Growth Factor beta1; D003094:Collagen