Monocyte-derived inflammatory Langerhans cells and dermal dendritic cells mediate psoriasis-like inflammation

Tej Pratap Singh, Howard H. Zhang, Izabela Borek, Peter Wolf, Michael N. Hedrick, Satya P. Singh, Brian L. Kelsall, Bjorn E. Clausen and Joshua M. Farber ()
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Tej Pratap Singh: Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, US National Institutes of Health
Howard H. Zhang: Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, US National Institutes of Health
Izabela Borek: Institute of Pathophysiology and Immunology, Medical University of Graz
Peter Wolf: Medical University of Graz
Michael N. Hedrick: Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, US National Institutes of Health
Satya P. Singh: Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, US National Institutes of Health
Brian L. Kelsall: Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, US National Institutes of Health
Bjorn E. Clausen: Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz
Joshua M. Farber: Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, US National Institutes of Health

Nature Communications, 2016, vol. 7, issue 1, 1-18

Abstract: Abstract Dendritic cells (DCs) have been implicated in the pathogenesis of psoriasis but the roles for specific DC subsets are not well defined. Here we show that DCs are required for psoriasis-like changes in mouse skin induced by the local injection of IL-23. However, Flt3L-dependent DCs and resident Langerhans cells are dispensable for the inflammation. In epidermis and dermis, the critical DCs are TNF-producing and IL-1β-producing monocyte-derived DCs, including a population of inflammatory Langerhans cells. Depleting Ly6Chi blood monocytes reduces DC accumulation and the skin changes induced either by injecting IL-23 or by application of the TLR7 agonist imiquimod. Moreover, we find that IL-23-induced inflammation requires expression of CCR6 by DCs or their precursors, and that CCR6 mediates monocyte trafficking into inflamed skin. Collectively, our results imply that monocyte-derived cells are critical contributors to psoriasis through production of inflammatory cytokines that augment the activation of skin T cells.

Date: 2016
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DOI: 10.1038/ncomms13581

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