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Epidermal Langerhans Cells Are Not Required for UV-Induced Immunosuppression¹

Center for Immunology, Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN 55455

UV light can be highly beneficial in the treatment of skin disorders such as psoriasis. It is thought to cause immunosuppression by depleting or altering the function of epidermal Langerhans cells (LC). Our previous studies identified a novel langerin⁺ dendritic cell in the dermis, distinct from LC in phenotype, circulation, and function. In this study, we determined the role of LC and dermal langerin⁺ cells in UV suppression. UV light suppressed the CD8 T cell response to both contact hypersensitivity and epicutaneous protein immunization, and resulted in a dramatically altered phenotype of LC. UV light did not alter early CD8 T cell activation in the lymph nodes, but rather reduced CD8 T cell expansion at later time points. We found that dermal langerin⁺ cells, but not LC, were essential for the CD8 T cell response. Furthermore, in the selective absence of LC, UV light still caused suppression of both CD8 T cell expansion and contact hypersensitivity.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by Grants P01 AI 35296 (to K.A.H.) and U01 AI 70380 (to S.C.J.) from the National Institutes of Health.

² Address correspondence and reprint requests to Dr. Kristin A. Hogquist, Center for Immunology, Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN 55455. E-mail address: hogqu001{at}umn.edu

³ Abbreviations used in this paper: CHS, contact hypersensitivity; LC, Langerhans cell; DC, dendritic cell; EGFP, enhanced GFP; DTR, diphtheria toxin receptor.