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Transcription-Coupled and Global Genome Repair Differentially Influence UV-B-Induced Acute Skin Effects and Systemic Immunosuppression¹

Johan Garssen^2,*, Harry van Steeg, Frank de Gruijl, Jan de Boer^§, Gijsbertus T. J. van der Horst^§, Henk van Kranen, Henk van Loveren^*, Mariska van Dijk^*, Angelique Fluitman^*, Geert Weeda^§ and Jan H. J. Hoeijmakers^§

^* Laboratory for Pathology and Immunobiology and Laboratory of Health Effects Research, National Institute of Public Health and the Environment, Bilthoven, The Netherlands; Department of Dermatology, Utrecht University, Utrecht, The Netherlands; and ^§ MGC-Department of Cell Biology and Genetics, Center for Biomedical Genetics, Erasmus University, Rotterdam, The Netherlands

Exposure to UV-B radiation impairs immune responses in mammals by inhibiting especially Th1-mediated contact hypersensitivity and delayed-type hypersensitivity. Immunomodulation is not restricted to the exposed skin, but is also observed at distant sites, indicating the existence of mediating factors such as products from exposed skin cells or photoactivated factors present in the superficial layers. DNA damage appears to play a key role, because enhanced nucleotide excision repair (NER) strongly counteracts immunosuppression. To determine the effects of the type and genomic location of UV-induced DNA damage on immunosuppression and acute skin reactions (edema and erythema) four congenic mouse strains carrying different defects in NER were compared: CSB and XPC mice lacking transcription-coupled or global genome NER, respectively, as well as XPA and TTD/XPD mice carrying complete or partial defects in both NER subpathways, respectively. The major conclusions are that 1) transcription-coupled DNA repair is the dominant determinant in protection against acute skin effects; 2) systemic immunomodulation is only affected when both NER subpathways are compromised; and 3) sunburn is not related to UV-B-induced immunosuppression.

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