期刊
AMERICAN JOURNAL OF PATHOLOGY
卷 169, 期 3, 页码 795-805出版社
ELSEVIER SCIENCE INC
DOI: 10.2353/ajpath.2006.060079
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资金
- NCI NIH HHS [P30 CA016672, R01 CA131207-04, R01 CA112660, R01 CA131207, CA16672, CA75575, R01 CA131207-03, R01 CA075575, R01 CA046523, CA46523, CA88943, CA112660, R01 CA088943] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA112660, R01CA075575, R01CA046523, R01CA088943, P30CA016672, R01CA131207] Funding Source: NIH RePORTER
Psoralen plus UVA (PUVA) is used as a very effective treatment modality for various diseases, including psoriasis and cutaneous T-cell lymphoma. PUVA-induced immune suppression and/or apoptosis are thought to be responsible for the therapeutic action. However, the molecular mechanisms by which PUVA acts are not well understood. We have previously identified platelet-activating factor (PAF), a potent phospholipid mediator, as a crucial substance triggering ultraviolet B radiation-induced immune suppression. In this study, we used PAF receptor knockout mice, a selective PAF receptor antagonist, a COX-2 inhibitor (presumably blocking downstream effects of PAF), and PAF-like molecules to test the role of PAF receptor binding in PUVA treatment. we found that activation of the PAF pathway is crucial for PUVA-induced immune suppression (as measured by suppression of delayed type hypersensitivity to Candida albicans) and that it plays a role in skin inflammation and apoptosis. Downstream of PAF, interleukin-10 was involved in PUVA-induced immune suppression but not inflammation. Better understanding of PUVA's mechanisms may offer the opportunity to dissect the therapeutic from the detrimental (ie, carcinogenic) effects and/or to develop new drugs (eg, using the PAF pathway) that act like PUVA but have fewer side effects.
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