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Blood, 15 December 2004, Vol. 104, No. 13, pp. 4038-4045.
Prepublished online as a Blood First Edition Paper on August 10, 2004; DOI 10.1182/blood-2004-03-1140.
Previous Article | Next Article 
Submitted March 25, 2004
Accepted July 26, 2004
Dectin-1 utilizes novel mechanisms for yeast phagocytosis in macrophages
Jurgen Herre, Andrew S Marshall, Emmanuelle Caron, Alexander D Edwards, David L Williams, Edina Schweighoffer, Victor Tybulewicz, Caetano Reis e Sousa, Siamon Gordon, and Gordon D Brown*
Sir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom
Centre for Molecular Microbiology and Infection and Department of Biological Sciences, Imperial College, London, United Kingdom
Immunobiology Laboratory, Cancer Research UK, London, United Kingdom
Department of Surgery, James H. Quillen College of Medicine, Johnson City, USA
National Institute for Medical Research, London, United Kingdom
Sir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom; Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Cape Town, South Africa
* Corresponding author; email: gordon.brown{at}mweb.co.za.
The phagocytosis of pathogens is a critical event in host defence, not only for clearance of the invading micro-organism, but also for the subsequent immune response. We have examined Dectin-1, a pro-inflammatory non-opsonic receptor for -glucans, and show that it mediates the internalisation of -glucan bearing ligands, including yeast particles. Although requiring tyrosine phosphorylation and the cytoplasmic ITAM-like motif, uptake mediated by Dectin-1 was different to any previously reported phagocytic receptor and was not dependent on Syk-kinase in macrophages. Furthermore, intracellular trafficking of this receptor was influenced by the nature of the -glucan ligand, which has significance for the biological activity of these immunomodulatory carbohydrates.

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