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Photochem Photobiol. 2010 Jan-Feb;86(1):231-5. doi: 10.1111/j.1751-1097.2009.00618.x. Epub 2009 Sep 21.

Epidermal platelet-activating factor receptor activation and ultraviolet B radiation result in synergistic tumor necrosis factor-alpha production.

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  • 1Department of Dermatology, Indiana University School of Medicine, Indianapolis, IN, USA.


Ultraviolet B radiation (UVB) is a potent stimulator of epidermal cytokine production which has been implicated in photoaggravated dermatoses. In addition to cytokines such as tumor necrosis factor-alpha (TNF-alpha), UVB generates bioactive lipids including platelet-activating factor (PAF). Our previous studies have demonstrated that UVB-mediated production of keratinocyte TNF-alpha is in part due to PAF. The current studies use a human PAF-receptor (PAF-R) negative epithelial cell line transduced with PAF-Rs and PAF-R-deficient mice to demonstrate that activation of the epidermal PAF-R along with UVB irradiation results in a synergistic production of TNF-alpha. It should be noted that PAF-R effects are mimicked by the protein kinase C (PKC) agonist phorbol myristic acetate, and are inhibited by pharmacological antagonists of the PKC gamma isoenzyme. These studies suggest that concomitant PAF-R activation and UVB irradiation results in a synergistic production of the cytokine TNF-alpha which is mediated in part via PKC. These studies provide a novel potential mechanism for photosensitivity responses.

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