The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
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© The Rockefeller University Press, 0022-1007/1997/11/1757/ $5.00
The Journal of Experimental Medicine, Volume 186, Number 10, November 17, 1997 1757-1762

Brief Definitive Reports

Defects in Macrophage Recruitment and Host Defense in Mice Lacking the CCR2 Chemokine Receptor

Takao Kurihara*, Glenn Warr§, James Loy{ddagger}, and Rodrigo Bravo*

From the Department of * Oncology and {ddagger} Experimental Pathology, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, New Jersey 08543-4000; and the § Department of Microbiology, Bristol-Myers Squibb Pharmaceutical Research Institute, Wallingford, Connecticut 06492-7660

Chemokines are a structurally related family of cytokines that are important for leukocyte trafficking. The C-C chemokine monocyte chemoattractant protein-1 (MCP-1) is a potent monocyte activator in vitro and has been associated with monocytic infiltration in several inflammatory diseases. One C-C chemokine receptor, CCR2, has been identified that mediates in vitro responses to MCP-1 and its close structural homologues. CCR2 has also recently been demonstrated to be a fusion cofactor for several HIV isolates. To investigate the normal physiological function of CCR2, we generated mice with a targeted disruption of the ccr2 gene. Mice deficient for CCR2 developed normally and had no hematopoietic abnormalities. However, ccr2–/– mice failed to recruit macrophages in an experimental peritoneal inflammation model. In addition, these mice were unable to clear infection by the intracellular bacteria, Listeria monocytogenes. These results suggest that CCR2 has a nonredundant role as a major mediator of macrophage recruitment and host defense against bacterial pathogens and that MCP-1 and other CCR2 ligands are effectors of those functions.

Address correspondence to Rodrigo Bravo, Department of Oncology Bristol-Myers Squibb Pharmaceutical Research Institute P.O. Box 4000, Princeton, New Jersey 08543-4000. Phone: (609) 252-5744; Fax: (609) 252-6051.


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