Published online before print February 21, 2008

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Copyright © 2008 American Society for Investigative Pathology
American Journal of Pathology, doi:10.2353/ajpath.2008.070517

Accepted for publication December 18, 2007.

Article

Ultraviolet B Suppresses Immunity by Inhibiting Effector and Memory T Cells

From the Department of Medicine, Melanoma and Skin Cancer Research Institute, Sydney Cancer Centre, The University of Sydney, Sydney, Australia

^@ To whom correspondence should be addressed. E-mail: garyh{at}med.usyd.edu.au.

	Abstract

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-⁺ 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.