Skin-resident T cells sense ultraviolet radiation-induced injury and contribute to DNA repair.
Journal Article (Clinical Trial;Journal Article)
Skin-resident T cells have been shown to play important roles in tissue homeostasis and wound repair, but their role in UV radiation (UVR)-mediated skin injury and subsequent tissue regeneration is less clear. In this study, we demonstrate that acute UVR rapidly activates skin-resident T cells in humans and dendritic epidermal γδ T cells (DETCs) in mice through mechanisms involving the release of ATP from keratinocytes. Following UVR, extracellular ATP leads to an increase in CD69 expression, proliferation, and IL-17 production, and to changes in DETC morphology. Furthermore, we find that the purinergic receptor P2X7 and caspase-1 are necessary for UVR-induced IL-1 production in keratinocytes, which increases IL-17 secretion by DETCs. IL-17, in turn, induces epidermal TNF-related weak inducer of apoptosis and growth arrest and DNA damage-associated gene 45, two molecules linked to the DNA repair response. Finally, we demonstrate that DETCs and human skin-resident T cells limit DNA damage in keratinocytes. Taken together, our findings establish a novel role for skin-resident T cells in the UVR-associated DNA repair response and underscore the importance of skin-resident T cells to overall skin regeneration.
Full Text
Duke Authors
Cited Authors
- MacLeod, AS; Rudolph, R; Corriden, R; Ye, I; Garijo, O; Havran, WL
Published Date
- June 15, 2014
Published In
Volume / Issue
- 192 / 12
Start / End Page
- 5695 - 5702
PubMed ID
- 24808367
Pubmed Central ID
- PMC4048764
Electronic International Standard Serial Number (EISSN)
- 1550-6606
Digital Object Identifier (DOI)
- 10.4049/jimmunol.1303297
Language
- eng
Conference Location
- United States