Journal
JOURNAL OF INVESTIGATIVE DERMATOLOGY
Volume 134, Issue 8, Pages 2231-2240Publisher
ELSEVIER SCIENCE INC
DOI: 10.1038/jid.2014.153
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Funding
- US National Institutes of Health [AI074957]
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UVB is a component of solar radiation primarily responsible for causing damage and cancer in irradiated skin, and disrupting immune homeostasis. The immediate harm and long-term health risks of excessive sunlight exposure are affecting the lives of nearly all people worldwide. Inflammation is a key mechanism underlying UVB's various detrimental effects. Here we show that activation of the protein kinase p38 alpha, is restricted to the epidermis in UVB-exposed skin, and that p38 alpha ablation targeted to the epithelial compartment is sufficient to suppress UVB-induced inflammation. Mechanistically, loss of epithelial p38 alpha signaling attenuates the expression of genes required to induce vascular leakage and edema, and also increases the steady-state abundance of epidermal gamma delta T cells, which are known to promote the repair of damaged epidermis. These effects of p38 alpha deficiency delineate a molecular network operating at the organism environment interface, and reveal conditions crucial to preventing the pathology resulting from sun-damaged skin.
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