Skin-resident T cells sense ultraviolet radiation-induced injury and contribute to DNA repair.
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.
Duke Scholars
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Related Subject Headings
- Ultraviolet Rays
- Tumor Necrosis Factor-alpha
- T-Lymphocytes
- Regeneration
- Receptors, Antigen, T-Cell, gamma-delta
- Mice, Knockout
- Mice
- Male
- Lectins, C-Type
- Keratinocytes
Citation
Published In
DOI
EISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Ultraviolet Rays
- Tumor Necrosis Factor-alpha
- T-Lymphocytes
- Regeneration
- Receptors, Antigen, T-Cell, gamma-delta
- Mice, Knockout
- Mice
- Male
- Lectins, C-Type
- Keratinocytes