Published online
doi:10.1084/jem.20081787
The Journal of Experimental Medicine, Vol. 206, No. 4, 743-750
The Rockefeller University Press, 0022-1007 $30.00
© Toulon et al.
A role for human skin–resident T cells in wound healing
Antoine Toulon1,
Lionel Breton3,
Kristen R. Taylor1,
Mayer Tenenhaus4,
Dhaval Bhavsar4,
Caroline Lanigan2,
Ross Rudolph4,5,
Julie Jameson1, and
Wendy L. Havran1,6
1 Department of Immunology and Microbial Science and 2 Department of Molecular and Integrative Neurosciences, The Scripps Research Institute, La Jolla, CA 92037
3 L'Oréal Recherche, 92583 Clichy, France
4 Division of Plastic Surgery, University of California, San Diego, San Diego, CA 92103
5 Division of Plastic Surgery, Scripps Clinic, La Jolla, CA 92037
6 Division of Dermatology, University of California, San Diego, La Jolla, CA 92037
CORRESPONDENCE Wendy L. Havran: havran{at}scripps.edu
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
β+ and 
+ 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
β+ and V
1+ 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.
© 2009 Toulon et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).
© 2009 Toulon et al.
This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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