J. Exp. Med., Volume 187, Number 4, February 16, 1998 601-608

Abnormalities in Monocyte Recruitment and Cytokine Expression in Monocyte Chemoattractant Protein 1-deficient Mice

By Bao Lu, Barbara J. Rutledge,^* Long Gu,^* Joseph Fiorillo,^* Nicholas W. Lukacs,^§ Steven L. Kunkel,^§ Robert North,^¶ Craig Gerard, and Barrett J. Rollins^*

From the ^* Department of Adult Oncology, Dana-Farber Cancer Institute, and the  Perlmutter Laboratory, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115; the ^§ Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan 48105; and the ^¶ Trudeau Institute, Saranac Lake, New York 12983

Monocyte chemoattractant protein 1 (MCP-1) is a CC chemokine that attracts monocytes, memory T lymphocytes, and natural killer cells. Because other chemokines have similar target cell specificities and because CCR2, a cloned MCP-1 receptor, binds other ligands, it has been uncertain whether MCP-1 plays a unique role in recruiting mononuclear cells in vivo. To address this question, we disrupted SCYA2 (the gene encoding MCP-1) and tested MCP-1-deficient mice in models of inflammation. Despite normal numbers of circulating leukocytes and resident macrophages, MCP-1^/ mice were specifically unable to recruit monocytes 72 h after intraperitoneal thioglycollate administration. Similarly, accumulation of F4/80+ monocytes in delayed-type hypersensitivity lesions was impaired, although the swelling response was normal. Development of secondary pulmonary granulomata in response to Schistosoma mansoni eggs was blunted in MCP-1^/ mice, as was expression of IL-4, IL-5, and interferon  in splenocytes. In contrast, MCP-1^/ mice were indistinguishable from wild-type mice in their ability to clear Mycobacterium tuberculosis. Our data indicate that MCP-1 is uniquely essential for monocyte recruitment in several inflammatory models in vivo and influences expression of cytokines related to T helper responses.

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