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* Institut de Recherche Interdisciplinaire en Biologie Humaine et Moléculaire, Université Libre de Bruxelles, Brussels, Belgium;
Service d’Anatomie Pathologique Erasme, Université Libre de Bruxelles, Brussels, Belgium;
Euroscreen SA, Gosselies, Belgium; and
Department of Biomedical Sciences and Biotechnologies, University of Brescia, Brescia, Italy
The formyl peptide receptor (FPR) is a key player in innate immunity and host defense mechanisms. In humans and other primates, a cluster of genes encodes two related receptors, FPR-like 1 and FPR-like 2 (FPRL1 and FPRL2). Despite their high sequence similarity, the three receptors respond to different sets of ligands and display a different expression pattern in leukocyte populations. Unlike FPR and FPRL1, FPRL2 is absent from neutrophils, and two endogenous peptide agonists, F2L and humanin, were recently described. In the present work, we investigated the detailed functional distribution of FPRL2 in leukocytes by quantitative PCR, flow cytometry, immunohistochemistry, and chemotaxis assays, with the aim of raising hypotheses regarding its potential functions in the human body. We describe that FPRL2 is highly expressed and functional in plasmacytoid dendritic cells and up-regulated upon their maturation. FPRL2 is also expressed in eosinophils, which are recruited but do not degranulate in response to F2L. FPRL2 is expressed and functional in macrophages differentiated from monocytes in vitro in different conditions. However, in vivo, only specific subsets of macrophages express the receptor, particularly in the lung, colon, and skin, three organs chronically exposed to pathogens and exogenous aggressions. This distribution and the demonstration of the production of the F2L peptide in mice underline the potential role of FPRL2 in innate immunity and possibly in immune regulation and allergic diseases.
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1 This work was supported by the Actions de Recherche Concertées of the Communauté Française de Belgique, the Interuniversity Attraction Poles Programme-Belgian State-Belgian Science Policy, the European Union (Grant LSHB-CT-2005-518167/INNOCHEM), the Fonds de la Recherche Scientifique Médicale of Belgium, the Walloon Region (Programme d’excellence CIBLES), the Fédération Belge contre le Cancer, the Fonds Ithier and the Fondation Médicale Reine Elisabeth, the Fonds Yvonne Boël, and grants from the Italian Ministero dell’istruzione, Università e Ricerca (PRIN projects) and AIRC (Associazione Italiana per la Ricerca sul Cancro). T.D. is an Aspirant of the National Fund for Scientific Research of Belgium.
2 Address correspondence and reprint requests to Dr. Marc Parmentier, Institut de Recherche Interdisciplinaire en Biologie Humaine et Moléculaire, Université Libre de Bruxelles, Campus Erasme, Route de Lennik 808, B-1070, Brussels, Belgium. E-mail address: mparment{at}ulb.ac.be
3 Abbreviations used in this paper: FPR, formyl peptide receptor; FPRL1, FPR-like 1; FPRL2, FPR-like 2; DC, dendritic cell; hF2L, human F2L; mF2L; mouse F2L; Fpr-rs, Fpr-related sequence; rh, recombinant human; HEBP1, heme-binding protein-1; SDF-1, stromal cell-derived factor-1; pDC, plasmacytoid DC; ROS, reactive oxygen species; TFA, trifluoroacetic acid; CHO, Chinese hamster ovary; MGC, multinucleated giant cell; TAM, tumor-associated macrophage.
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  C. Prat, P.-J. Haas, J. Bestebroer, C. J. C. de Haas, J. A. G. van Strijp, and K. P. M. van Kessel A Homolog of Formyl Peptide Receptor-Like 1 (FPRL1) Inhibitor from Staphylococcus aureus (FPRL1 Inhibitory Protein) That Inhibits FPRL1 and FPR J. Immunol., November 15, 2009; 183(10): 6569 - 6578. [Abstract] [Full Text] [PDF]
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