Sano, YasuyoPark, Jin Mo2015-03-022014Sano, Yasuyo, and Jin Mo Park. 2014. “Loss of epidermal p38α signaling prevents ultraviolet radiation-induced inflammation via acute and chronic mechanisms.” The Journal of investigative dermatology 134 (8): 2231-2240. doi:10.1038/jid.2014.153. http://dx.doi.org/10.1038/jid.2014.153.0022-202Xhttp://nrs.harvard.edu/urn-3:HUL.InstRepos:14065555Ultraviolet B radiation (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 impacting 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 p38α is restricted to the epidermis in UVB-exposed skin, and p38α ablation targeted to the epithelial compartment is sufficient to suppress UVB-induced inflammation. Mechanistically, loss of epithelial p38α signaling attenuates the expression of genes required to induce vascular leakage and edema, and also increases the steady-state abundance of epidermal γδ T cells, which are known to promote the repair of damaged epidermis. These effects of p38α deficiency delineate a molecular network operating at the organism-environment interface, and reveal conditions crucial to preventing the pathology resulting from sun-damaged skin.en-USJournal Article2015-03-0210.1038/jid.2014.153