A role for human skin-resident T cells in wound healing.
Epidermal T cells have been shown to play unique roles in tissue homeostasis and repair in mice through local secretion of distinct growth factors in the skin. Human epidermis contains both alphabeta(+) and gammadelta(+) T cells whose functional capabilities are not understood. We demonstrate that human epidermal T cells are able to produce insulin-like growth factor 1 (IGF-1) upon activation and promote wound healing in a skin organ culture model. Moreover, an analysis of the functional capabilities of T cells isolated from acute versus chronic wounds revealed a striking difference. Both alphabeta(+) and Vdelta1(+) T cells isolated from acute wounds actively produced IGF-1, demonstrating that they are activated during tissue damage to participate in wound repair. In contrast, IGF-1 production could not be detected in T cells isolated from chronic wounds. In fact, skin T cells isolated from chronic wounds were refractory to further stimulation, suggesting an unresponsive state. Collectively, these results define a novel role for human epidermis-resident T cells in wound healing and provide new insight into our understanding of chronic wound persistence.
Toulon
Antoine
A
Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA.
Breton
Lionel
L
Taylor
Kristen R
KR
Tenenhaus
Mayer
M
Bhavsar
Dhaval
D
Lanigan
Caroline
C
Rudolph
Ross
R
Jameson
Julie
J
Havran
Wendy L
WL
D002908:Chronic Disease; D004817:Epidermis / Q000276:immunology* / Q000502:physiology; D005434:Flow Cytometry; D052816:Foreskin / Q000276:immunology / Q000502:physiology; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000096:biosynthesis / Q000502:physiology; D008213:Lymphocyte Activation; D008297:Male; D009924:Organ Culture Techniques; D012867:Skin / Q000276:immunology; D012879:Skin Physiological Phenomena; D013601:T-Lymphocytes / Q000276:immunology* / Q000502:physiology; D014945:Wound Healing / Q000276:immunology*
D007334:Insulin-Like Growth Factor I