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¹ Department of Laboratory Medicine and Pathology, ² Department of Dermatology, and ³ Center for Immunology, University of Minnesota, Minneapolis, MN 55455
⁴ Centre d'Immunologie de Marseille-Luminy, Institut National de la Santé et de la Recherche Médicale-Centre National de la Recherche Scientifique, Université de la Méditerranée Parc Scientifique et Technologique de Luminy, Case 906, 13288 Marseille, Cedex 09, France

CORRESPONDENCE Kristin A. Hogquist: hogqu001{at}umn.edu

Langerhans cells (LCs) are antigen-presenting cells that reside in the epidermis of the skin and traffic to lymph nodes (LNs). The general role of these cells in skin immune responses is not clear because distinct models of LC depletion resulted in opposite conclusions about their role in contact hypersensitivity (CHS) responses. While comparing these models, we discovered a novel population of LCs that resides in the dermis and does not represent migrating epidermal LCs, as previously thought. Unlike epidermal LCs, dermal Langerin⁺ dendritic cells (DCs) were radiosensitive and displayed a distinct cell surface phenotype. Dermal Langerin⁺ DCs migrate from the skin to the LNs after inflammation and in the steady state, and represent the majority of Langerin⁺ DCs in skin draining LNs. Both epidermal and dermal Langerin⁺ DCs were depleted by treatment with diphtheria toxin in Lang-DTREGFP knock-in mice. In contrast, transgenic hLang-DTA mice lack epidermal LCs, but have normal numbers of dermal Langerin⁺ DCs. CHS responses were abrogated upon depletion of both epidermal and dermal LCs, but were unaffected in the absence of only epidermal LCs. This suggests that dermal LCs can mediate CHS and provides an explanation for previous differences observed in the two-model systems.

A. Kissenpfennig's present address is Infection and Immunity Group, Centre for Cancer Research and Cell Biology, School of Biomedical Sciences, Queens University, Belfast, Northern Ireland.

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