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Differential Migration of Epidermal and Dermal Dendritic Cells during Skin Infection¹

Liv Eidsmo^*, Rhys Allan^*, Irina Caminschi, Nico van Rooijen, William R. Heath^2,*, and Francis R. Carbone^2,*

^* Department of Microbiology and Immunology, University of Melbourne, Melbourne Victoria, Australia; Division of Immunology, Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria, Australia; and Department of Molecular Cell Biology, Faculty of Medicine, Vrije Universiteit Medical Center, Amsterdam, The Netherlands

Dendritic cells (DCs) are extremely heterogeneous, most evident in the skin where a variety of different subsets have been identified in recent years. DCs of healthy skin include a number of distinct populations in the dermal layer as well as the well-characterized Langerhans cells (LCs) of the epidermis. These steady-state populations are augmented during bouts of local inflammation by additional monocyte-derived DCs. In an effort to better understand the distinction between the different subsets, we examined their behavior following skin infection with HSV. LC emigration rapidly followed appearance of virus in the skin and resulted in depopulation of regions in areas surrounding infected nerve endings. A separate DC population was found to accumulate within the dermis under patches of active epidermal infection with at least some derived from blood monocyte precursors. Ag-positive DCs could occasionally be found in these dermal accumulations, although they represented a minority of DCs in these areas. In addition, infected DCs appeared compromised in their trafficking capabilities and were largely absent from the migrating population. On resolution of skin disease, LCs repopulated the reformed epidermis and these were of mixed origin, with around half entering from the circulation and the remainder derived from local progenitors. Overall, our results show a range of migrational complexities between distinct skin DC populations as a consequence of localized infection.

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 from the National Health and Medical Research Council of Australia and the Howard Hughes Medical Institute. L.E. was supported by a Swedish Research Council Fellowship.

² Address correspondence and reprint requests to Dr. Francis Carbone and Dr. William R. Heath, Department of Microbiology and Immunology, University of Melbourne, 3010, Victoria, Australia. E-mail addresses: fcarbone{at}unimelb.edu.au and wrheath{at}unimelb.edu.au

³ Abbreviations used in this paper: DC, dendritic cell; LC, Langerhans cell; TRITC, tetramethylrhodamine isothiocyanate; MHCII, MHC class II; DAPI, 4',6-diamidino-2-phenylindole.