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¹ Istituto Dermopatico dell'Immacolata, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), 00167 Rome, Italy
² Department of Biomedical Sciences and Biotechnology, Section of General Pathology and Immunology, University of Brescia, 25123 Brescia, Italy
³ Department of Biomedical and Surgical Sciences, Section of Dermatology and Venereology, University of Verona, 37126 Verona, Italy
⁴ IRCCS Istituto Clinico Humanitas, 20089 Rozzano, Italy
⁵ Euroscreen s.a., 6041Gosselies, Belgium
⁶ Institut de Recherche Interdisciplinaire en Biologie Humaine et Moléculaire, Campus Erasme, 1070 Brussels, Belgium

CORRESPONDENCE Silvano Sozzani: sozzani{at}med.unibs.it

Psoriasis is a type I interferon-driven T cell–mediated disease characterized by the recruitment of plasmacytoid dendritic cells (pDC) into the skin. The molecules involved in pDC accumulation in psoriasis lesions are unknown. Chemerin is the only inflammatory chemotactic factor that is directly active on human blood pDC in vitro. The aim of this study was to evaluate the role of the chemerin/ChemR23 axis in the recruitment of pDC in psoriasis skin. Prepsoriatic skin adjacent to active lesions and early lesions were characterized by a strong expression of chemerin in the dermis and by the presence of CD15⁺ neutrophils and CD123⁺/BDCA-2⁺/ChemR23⁺ pDC. Conversely, skin from chronic plaques showed low chemerin expression, segregation of neutrophils to epidermal microabscesses, and few pDC in the dermis. Chemerin expression was localized mainly in fibroblasts, mast cells, and endothelial cells. Fibroblasts cultured from skin of psoriatic lesions expressed higher levels of chemerin messenger RNA and protein than fibroblasts from uninvolved psoriatic skin or healthy donors and promoted pDC migration in vitro in a chemerin-dependent manner. Therefore, chemerin expression specifically marks the early phases of evolving skin psoriatic lesions and is temporally strictly associated with pDC. These results support a role for the chemerin/ChemR23 axis in the early phases of psoriasis development.

G. Girolomoni and S. Sozzani contributed equally to this paper.

© 2009 Albanesi et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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