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CLEC-2 Is a Phagocytic Activation Receptor Expressed on Murine Peripheral Blood Neutrophils¹

Ann M. Kerrigan^*, Kevin M. Dennehy^2,*, Diego Mourão-Sá, Inês Faro-Trindade^*, Janet A. Willment^*, Philip R. Taylor, Johannes A. Eble, Caetano Reis e Sousa and Gordon D. Brown^3,*

^* Institute of Infectious Disease and Molecular Medicine, Clinical Laboratory Sciences, Division of Immunology, University of Cape Town, Cape Town, South Africa, Immunobiology Laboratory, Cancer Research U.K., London Research Institute, London, United Kingdom; Department of Medical Biochemistry and Immunology, Cardiff University School of Medicine, Cardiff, United Kingdom, and Center for Molecular Medicine, Department of Vascular Matrix Biology, Excellence Cluster Cardio-Pulmonary System, Frankfurt University Hospital, Frankfurt, Germany

CLEC-2 is a member of the "dectin-1 cluster" of C-type lectin-like receptors and was originally thought to be restricted to platelets. In this study, we demonstrate that murine CLEC-2 is also expressed by peripheral blood neutrophils, but only weakly by bone marrow or elicited inflammatory neutrophils. On circulating neutrophils, CLEC-2 can mediate phagocytosis of Ab-coated beads and the production of proinflammatory cytokines, including TNF-, in response to the CLEC-2 ligand, rhodocytin. CLEC-2 possesses a tyrosine-based cytoplasmic motif similar to that of dectin-1, and we show using chimeric analyses that the activities of this receptor are dependent on this tyrosine. Like dectin-1, CLEC-2 can recruit the signaling kinase Syk in myeloid cells, however, stimulation of this pathway does not induce the respiratory burst. These data therefore demonstrate that CLEC-2 expression is not restricted to platelets and that it functions as an activation receptor on neutrophils.

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 the National Research Foundation (South Africa), the University of Cape Town and the Wellcome Trust. D.M.S. and C.R.C. are supported by Cancer Research U.K. J.A.E. is financially supported by the German Research Council (DFG Grant Eb 177/5-1). P.R.T. is an MRC Senior Research Fellow (G0601617). G.D.B. is a Wellcome Trust Senior Research Fellow in Biomedical Science in South Africa.

² Current address: Department of Immunology, Institute for Cell Biology, Eberhard Karls University of Tübingen, Tübingen, Germany.

³ Address correspondence and reprint requests to Professor Gordon D. Brown, Institute of Infectious Disease and Molecular Medicine, Clinical Laboratory Sciences, Division of Immunology, University of Cape Town, Observatory 7925, Cape Town, South Africa. E-mail address: gordon.brown{at}mweb.co.za

⁴ Abbreviations used in this paper: CRD, carbohydrate recognition domain; CLEC, C-type lectin like receptor; mCLEC-2, murine CLEC-2; HA, hemaggluglutinin.

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