{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T16:16:01Z","timestamp":1781108161259,"version":"3.54.1"},"reference-count":37,"publisher":"National Academy of Sciences","issue":"48","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2007,11,27]]},"abstract":"<jats:p>\n                    Terrestrial solar UVB radiation (\u2248295\u2013320 nm) readily induces cyclobutane pyrimidine dimers (CPDs) in human skin DNA that result in characteristic mutations associated with nonmelanoma skin cancer. The proinflammatory cytokine TNF\u03b1 is important in mouse skin chemical carcinogenesis and is thought to also play a role in UVR-induced skin cancer by its immunomodulatory properties. There is some\n                    <jats:italic>in vitro<\/jats:italic>\n                    evidence that CPDs initiate the production of TNF\u03b1, and we tested this hypothesis by comparing the wavelength dependence (action spectrum) for TNF\u03b1 protein induction in human skin\n                    <jats:italic>in vivo<\/jats:italic>\n                    with our earlier\n                    <jats:italic>in vivo<\/jats:italic>\n                    action spectra for CPD induction in four different epidermal layers of human skin. Normal volunteers (\n                    <jats:italic>n<\/jats:italic>\n                    = 35) were irradiated with physiologically relevant doses of monochromatic UVB (290\u2013320 nm), and TNF\u03b1 concentration was assessed, by high-sensitivity ELISA, in exudates from skin suction blisters raised 8 h after irradiation. An action spectrum, constructed from the slopes of the dose\u2013response curves at the different wavelengths, showed maximal efficacy at 300 nm. An excellent match was observed for TNF\u03b1 and the CPD action spectrum for cells in the lower basal epidermis. These data strongly suggest that UVB-induced photodamage to DNA in the epidermal basal layer is a major trigger for TNF\u03b1 production. The TNF\u03b1 may originate directly from the keratinocytes in this layer or inflammatory cells that are rapidly recruited into the upper dermis (e.g., neutrophils) as a consequence of DNA photodamage to basal-layer keratinocytes.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0703385104","type":"journal-article","created":{"date-parts":[[2007,11,19]],"date-time":"2007-11-19T21:15:10Z","timestamp":1195506910000},"page":"19051-19054","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":26,"title":["An action spectrum (290\u2013320 nm) for TNF\u03b1 protein in human skin\n                    <i>in vivo<\/i>\n                    suggests that basal-layer epidermal DNA is the chromophore"],"prefix":"10.1073","volume":"104","author":[{"given":"Susan L.","family":"Walker","sequence":"first","affiliation":[{"name":"St. John's Institute of Dermatology, Division of Genetics and Molecular Medicine, King's College London School of Medicine, 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