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


  • eng

Conference Location

  • United States