{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T01:04:16Z","timestamp":1790471056025,"version":"4.1.0"},"reference-count":22,"publisher":"Rockefeller University Press","issue":"3","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2000,2,7]]},"abstract":"<jats:p>Skin cancer incidence is highest in white-skinned people. Within this group, skin types I\/II (sun sensitive\/tan poorly) are at greater risk than skin types III\/IV (sun tolerant\/tan well). Studies in mice demonstrate that ultraviolet radiation (UVR)-induced suppression of cell-mediated immune function plays an important role in the development of skin cancer and induces a susceptibility to infectious disease. A similar role is suspected in humans, but we lack quantitative human data to make risk assessments of ambient solar exposure on human health. This study demonstrates that ambient levels of solar UVR, typically experienced within 1 h of exposure to noonday summer sunlight, can suppress contact hypersensitivity (CHS) responses in healthy white-skinned humans in vivo (n = 93). There was a linear relationship between increase in erythema and suppression of CHS (P &amp;lt; 0.001), and a moderate sunburn (two minimal erythema doses [2 MED]) was sufficient to suppress CHS in all volunteers by 93%. However, a single suberythemal exposure of either 0.25 or 0.5 MED suppressed CHS responses by 50 and 80%, respectively, in skin types I\/II, whereas 1 MED only suppressed CHS by 40% in skin types III\/IV. The two- to threefold greater sensitivity of skin types I\/II for a given level of sunburn may play a role in their greater sensitivity to skin cancer.<\/jats:p>","DOI":"10.1084\/jem.191.3.561","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T12:48:33Z","timestamp":1027687713000},"page":"561-566","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":149,"title":["Sensitivity to Sunburn Is Associated with Susceptibility to Ultraviolet Radiation\u2013Induced Suppression of Cutaneous Cell\u2013Mediated Immunity"],"prefix":"10.1084","volume":"191","author":[{"given":"Deirdre A.","family":"Kelly","sequence":"first","affiliation":[{"name":"aDepartment of Photobiology, St. John's Institute of Dermatology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antony R.","family":"Young","sequence":"additional","affiliation":[{"name":"aDepartment of Photobiology, St. John's Institute of Dermatology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jane M.","family":"McGregor","sequence":"additional","affiliation":[{"name":"aDepartment of Photobiology, St. John's Institute of Dermatology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul T.","family":"Seed","sequence":"additional","affiliation":[{"name":"bDepartment of Public Health Sciences, Guy's, King's, and St. Thomas' School of Medicine, King's College London, St. Thomas' Hospital, London SE1 7EH, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher S.","family":"Potten","sequence":"additional","affiliation":[{"name":"cCancer Research Campaign Department of Epithelial Biology, Paterson Institute for Cancer Research, Christie Hospital National Health Service Trust, Manchester M20 9BX, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Susan L.","family":"Walker","sequence":"additional","affiliation":[{"name":"aDepartment of Photobiology, St. John's Institute of Dermatology,"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","reference":[{"key":"2023072509015656700_R1","doi-asserted-by":"crossref","first-page":"583","DOI":"10.1016\/S0733-8635(18)30064-0","article-title":"Skin cancer","volume":"13","author":"Armstrong","year":"1995","journal-title":"Dermatol. 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