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    Am J Pathol. 2008 Apr;172(4):993-1004. Epub 2008 Feb 21.

    Ultraviolet B suppresses immunity by inhibiting effector and memory T cells.

    Rana S, Byrne SN, MacDonald LJ, Chan CY, Halliday GM.

    Department of Medicine, Melanoma and Skin Cancer Research Institute, Sydney Cancer Centre, The University of Sydney, NSW 2006, Australia.

    Contact hypersensitivity is a T-cell-mediated response to a hapten. Exposing C57BL/6 mice to UV B radiation systemically suppresses both primary and secondary contact hypersensitivity responses. The effects of UVB on in vivo T-cell responses during UVB-induced immunosuppression are unknown. We show here that UVB exposure, before contact sensitization, inhibits the expansion of effector CD4+ and CD8+ T cells in skin-draining lymph nodes and reduces the number of CD4+ and IFN-gamma+ CD8+ T cells infiltrating challenged ear skin. In the absence of UVB, at 10 weeks after initial hapten exposure, the ear skin of sensitized mice was infiltrated by dermal effector memory CD8+ T cells at the site of challenge. However, if mice were previously exposed to UVB, this cell population was absent, suggesting an impaired development of peripheral memory T cells. This finding occurred in the absence of UVB-induced regulatory CD4+ T cells and did not involve prostaglandin E2, suggesting that the importance of these two factors in mediating or initiating UVB-induced immunosuppression is dependent on UVB dose. Together these data indicate that in vivo T-cell responses are prone to immunoregulation by UVB, including a novel effect on both the activated T-cell pool size and the development of memory T cells in peripheral compartments.

    PMID: 18292235 [PubMed - indexed for MEDLINE]

    PMCID: 2276424

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