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Blood, 1 May 2007, Vol. 109, No. 9, pp. 3625-3632. Prepublished online as a Blood First Edition Paper on January 3, 2007; DOI 10.1182/blood-2006-08-038844. This Article Full Text (PDF) Supplemental Figure All Versions of this Article: blood-2006-08-038844v1 109/9/3625    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Parolini, S. Articles by Sozzani, S. Search for Related Content PubMed PubMed Citation Articles by Parolini, S. Articles by Sozzani, S. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted August 1, 2006 Accepted December 22, 2006 The role of chemerin in the co-localization of NK and dendritic cell subsets into inflamed tissues Silvia Parolini, Amerigo Santoro, Emanuela Marcenaro, Walter Luini, Luisa Massardi, Fabio Facchetti, David Communi, Marc Parmentier, Alessandra Majorana, Marina Sironi, Giovanna Tabellini, Alessandro Moretta, and Silvano Sozzani* Section of Histology, University of Brescia, Brescia, Italy Section of Pathology, University of Brescia, Brescia, Italy Dipartimento di Medicina Sperimentale, and Centro di Eccellenza per le Ricerche Biomediche, University of Genoa, Genoa, Italy Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy Section of General Pathology and Immunology, University of Brescia, Brescia, Italy Institut de Recherche Interdisciplinaire en Biologie Humaine, et Moleculaire, Universite Libre de Bruxelles, Brussels, Belgium Department of Dental Medicine, University of Brescia, Spedali Civili Brescia, Brescia, Italy Istituto Clinico Humanitas, Rozzano, Italy * Corresponding author; email: sozzani{at}med.unibs.it. Chemerin is a chemotactic agonist recently identified as the ligand of ChemR23, a serpentine receptor expressed by mononuclear phagocytes and dendritic cells. This study shows that blood CD56lowCD16+ NK cells selectively express functional ChemR23, and that this receptor is co-expressed with CXCR1, the CXCL8 receptor, and the KIR receptors. In vitro culturing of NK cells with IL-2 and IL-15 induced a delayed and time-dependent down-regulation of ChemR23 that was associated with the inhibition of NK cell migration to chemerin. Biopsies obtained from oral lichen planus patients presented an infiltration of CD94+CD3-CD56+ NK cells that co-expressed ChemR23. The same biopsies were infiltrated by myeloid, DC-SIGN+ and plasmacytoid, CD123+BDCA2+, ChemR23+ dendritic cells that were occasionally associated with NK cells. In the same histological sections, chemerin was expressed by inflamed dermal endothelium. These findings propose a role for the ChemR23/chemerin axis in the recruitment of blood NK cells and strongly implicate chemerin as a key factor for the co-localization of NK cells and DC subsets in pathological peripheral tissues. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. Tha-In, H. J. Metselaar, H. W. Tilanus, Z. M. A. Groothuismink, E. J. Kuipers, R. A. de Man, and J. Kwekkeboom Intravenous immunoglobulins suppress T-cell priming by modulating the bidirectional interaction between dendritic cells and natural killer cells Blood, November 1, 2007; 110(9): 3253 - 3262. [Abstract] [Full Text] [PDF]

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