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Previous studies have demonstrated that in addition to its known effects on keratinocytes and effector T cells, ultraviolet (\n                    <jats:styled-content style=\"fixed-case\">UV<\/jats:styled-content>\n                    ) irradiation alleviates psoriasis via the upregulation of\n                    <jats:styled-content style=\"fixed-case\">FOXP<\/jats:styled-content>\n                    3 + Tregs. However, the mechanism is unclear. Here, we found that\n                    <jats:styled-content style=\"fixed-case\">FOXP<\/jats:styled-content>\n                    3 + T cells were increased in psoriatic lesions after\n                    <jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content>\n                    irradiation (\n                    <jats:italic>t<\/jats:italic>\n                    ' = 3.7006,\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.01), as determined by immunohistochemical staining. In addition, the levels of\n                    <jats:styled-content style=\"fixed-case\">FOXP<\/jats:styled-content>\n                    3 and p53, one of the downstream targets of\n                    <jats:styled-content style=\"fixed-case\">UV<\/jats:styled-content>\n                    irradiation, showed accordant changes after\n                    <jats:styled-content style=\"fixed-case\">UV<\/jats:styled-content>\n                    irradiation. Experiments that used a\n                    <jats:styled-content style=\"fixed-case\">MAPK<\/jats:styled-content>\n                    inhibitor, p53 mutant cell lines, p53 inhibitor and p53 sh\n                    <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n                    showed a decrease in\n                    <jats:styled-content style=\"fixed-case\">FOXP<\/jats:styled-content>\n                    3 levels, suggesting that p53 is required for\n                    <jats:styled-content style=\"fixed-case\">UV<\/jats:styled-content>\n                    \u2010induced\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">FOXP<\/jats:styled-content>\n                      3\n                    <\/jats:italic>\n                    transcription. Next, we demonstrated that there are two binding sites for p53 on\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">FOXP<\/jats:styled-content>\n                      3\n                    <\/jats:italic>\n                    by informatics tools, a dual\u2010luciferase reporter assay and chromatin immunoprecipitation (ChIP) assay. One binding site (\u22121771 to \u22121583) is located at the promoter region and is adjacent to a previously reported p53\u2010binding region in breast cancer cells. The other (+3845 to +4042) is located within the first intron and has not been previously reported. Our study demonstrated that\n                    <jats:styled-content style=\"fixed-case\">FOXP<\/jats:styled-content>\n                    3 is regulated, at least in part, by the binding of p53 to several binding sites in the promoter and intron regions following\n                    <jats:styled-content style=\"fixed-case\">UV<\/jats:styled-content>\n                    irradiation in psoriasis. It will be helpful to further clarify the regulatory mechanism of\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">FOXP<\/jats:styled-content>\n                      3\n                    <\/jats:italic>\n                    transcription and to provide new insights into the mechanisms that mediate the effects of UV irradiation in autoimmune skin disorders.\n                  <\/jats:p>","DOI":"10.1111\/exd.12942","type":"journal-article","created":{"date-parts":[[2016,1,19]],"date-time":"2016-01-19T06:51:01Z","timestamp":1453186261000},"page":"513-518","source":"Crossref","is-referenced-by-count":27,"title":["Ultraviolet irradiation promotes\n                    <i>FOXP3<\/i>\n                    transcription via p53 in psoriasis"],"prefix":"10.1111","volume":"25","author":[{"given":"Dongmei","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Dermatology Southwest Hospital Third Military Medical University 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