Source:http://linkedlifedata.com/resource/pubmed/id/17363918
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2007-5-15
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pubmed:abstractText |
Solid organ transplant recipients have a 60-250-fold increased likelihood of developing sunlight-induced squamous cell carcinoma (SCC) compared with the general population. This increased risk is linked to the immunosuppressive drugs taken by these patients to modulate T cell function, thus preventing organ rejection. To determine the importance of T cells in the development of cutaneous SCC, we examined the effects of selectively depleting Skh-1 mice of systemic CD4+ or CD8+ T cells, using monoclonal antibodies, on ultraviolet B (UVB) radiation-induced inflammation and tumor development. Decreases in systemic CD4+ but not CD8+ T cells significantly increased and prolonged the acute UVB-induced cutaneous inflammatory response, as measured by neutrophil influx, myeloperoxidase activity, and prostaglandin E2 levels. Significantly more p53+ keratinocytes were observed in UVB-exposed CD4-depleted than in CD4-replete mice, and this difference was abrogated in mice depleted of neutrophils before UVB exposure. Increased acute inflammation was associated with significantly increased tumor numbers in CD4-depleted mice chronically exposed to UVB. Furthermore, topical treatment with the anti-inflammatory drug celecoxib significantly decreased tumor numbers in both CD4-replete and CD4-depleted mice. Our findings suggest that CD4+ T cells play an important role in modulating both the acute inflammatory and the chronic carcinogenic response of the skin to UVB.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1523-1747
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
127
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1507-15
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:17363918-Acute Disease,
pubmed-meshheading:17363918-Animals,
pubmed-meshheading:17363918-CD4-Positive T-Lymphocytes,
pubmed-meshheading:17363918-CD8-Positive T-Lymphocytes,
pubmed-meshheading:17363918-Chronic Disease,
pubmed-meshheading:17363918-Dermatitis,
pubmed-meshheading:17363918-Dinoprostone,
pubmed-meshheading:17363918-Female,
pubmed-meshheading:17363918-Immunocompromised Host,
pubmed-meshheading:17363918-Keratinocytes,
pubmed-meshheading:17363918-Mice,
pubmed-meshheading:17363918-Mice, Hairless,
pubmed-meshheading:17363918-Neutrophils,
pubmed-meshheading:17363918-Peroxidase,
pubmed-meshheading:17363918-Risk Factors,
pubmed-meshheading:17363918-Skin,
pubmed-meshheading:17363918-Skin Neoplasms,
pubmed-meshheading:17363918-Tumor Suppressor Protein p53,
pubmed-meshheading:17363918-Ultraviolet Rays
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pubmed:year |
2007
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pubmed:articleTitle |
Depletion of CD4+ cells exacerbates the cutaneous response to acute and chronic UVB exposure.
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pubmed:affiliation |
Department of Pathology, The Ohio State University, Columbus, Ohio, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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