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The Journal of Immunology, 2001, 167: 4585-4592.
Copyright © 2001 by The American Association of Immunologists

Lack of CCR2 Results in Increased Mortality and Impaired Leukocyte Activation and Trafficking Following Infection of the Central Nervous System with a Neurotropic Coronavirus1

Benjamin P. Chen*, William A. Kuziel{ddagger} and Thomas E. Lane2,*,{dagger}

* Department of Molecular Biology and Biochemistry and {dagger} Reeve-Irvine Research Center, University of California, Irvine, CA 92612; and {ddagger} Department of Molecular Genetics and Microbiology and Institute for Cellular and Molecular Biology, University of Texas, Austin, TX 78712

In the present study, we evaluated the role of CCR2 in a model of viral-induced neurologic disease. An orchestrated expression of chemokines, including the CCR2 ligands monocyte chemoattractant protein-1/CCL2 and monocyte chemoattractant protein-3/CCL7, occurs within the CNS following infection with mouse hepatitis virus (MHV). Infection of mice lacking CCR2 (CCR2-/-) with MHV resulted in increased mortality and enhanced viral recovery from the brain that correlated with reduced (p <= 0.04) T cell and macrophage/microglial (determined by F4/80 Ag expression, p <= 0.004) infiltration into the CNS. Moreover, MHV-infected CCR2-/- mice displayed a significant decrease in Th1-associated factors IFN-{gamma} (p <= 0.001) and RANTES/CCL5 (p <= 0.002) within the CNS as compared with CCR2+/+ mice. Further, peripheral CD4+ and CD8+ T cells from immunized CCR2-/- mice displayed a marked reduction in IFN-{gamma} production in response to viral Ag and did not migrate into the CNS of MHV-infected recombination-activating gene (RAG)1-/- mice following adoptive transfer. In addition, macrophage/microglial infiltration into the CNS of RAG1-/- mice receiving CCR2-/- splenocytes was reduced (p <= 0.05), which correlated with a reduction in the severity of demyelination (p <= 0.001) as compared with RAG1-/- mice receiving splenocytes from CCR2+/+ mice. Collectively, these results indicate an important role for CCR2 in host defense and disease by regulating leukocyte activation and trafficking.




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