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 Blood, 15 December 2008, Vol. 112, No. 13, pp. 5026-5036.
Prepublished online as a Blood First Edition Paper on September 17, 2008; DOI 10.1182/blood-2008-06-162404.

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IMMUNOBIOLOGY

CX3CL1/fractalkine is released from apoptotic lymphocytes to stimulate macrophage chemotaxis

Lucy A. Truman1,*, Catriona A. Ford1,*, Marta Pasikowska1, John D. Pound1, Sarah J. Wilkinson1, Ingrid E. Dumitriu1, Lynsey Melville1, Lauren A. Melrose1, Carol Anne Ogden1, Robert Nibbs2, Gerard Graham2, Christophe Combadiere3, and Christopher D. Gregory1

1 Medical Research Council (MRC) Centre for Inflammation Research, University of Edinburgh, Edinburgh, United Kingdom; 2 Division of Immunology, Infection, and Inflammation, University of Glasgow, Glasgow, United Kingdom; and 3 Laboratoire d'Immunologie Cellulaire, Faculte de Medecine Pitie-Salpetiere, Inserm U543, Paris, France

Cells undergoing apoptosis are efficiently located and engulfed by phagocytes. The mechanisms by which macrophages, the professional scavenging phagocytes of apoptotic cells, are attracted to sites of apoptosis are poorly defined. Here we show that CX3CL1/fractalkine, a chemokine and intercellular adhesion molecule, is released rapidly from apoptotic lymphocytes, via caspase- and Bcl-2-regulated mechanisms, to attract macrophages. Effective chemotaxis of macrophages to apoptotic lymphocytes is dependent on macrophage fractalkine receptor, CX3CR1. CX3CR1 deficiency caused diminished recruitment of macrophages to germinal centers of lymphoid follicles, sites of high-rate B-cell apoptosis. These results provide the first demonstration of chemokine/chemokine-receptor activity in the navigation of macrophages toward apoptotic cells and identify a mechanism by which macrophage infiltration of tissues containing apoptotic lymphocytes is achieved.


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