The Journal of Experimental Medicine
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Published online 18 September 2000.
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© The Rockefeller University Press, 0022-1007/2000/9/899/ $5.00
The Journal of Experimental Medicine, Volume 192, Number 6, September 18, 2000 899-906

Brief Definitive Report

Cc Chemokine Receptor 2 Is Critical for Induction of Experimental Autoimmune Encephalomyelitis

Brian T. Fifea, Gary B. Huffnagleb, William A. Kuzielc, and William J. Karpusa

a Department of Pathology, Northwestern University Medical School, Chicago, Illinois 60611
b Department of Medicine, University of Michigan Medical School, Ann Arbor, Michigan 48109
c Molecular Genetics and Microbiology, University of Texas, Austin, Texas 78712
Department of Pathology, Northwestern University Medical School, 303 E. Chicago Ave., W127, Chicago, IL 60611.312-503-1217312-503-1005

Experimental autoimmune encephalomyelitis (EAE) is a CD4+ T lymphocyte–mediated disease of the central nervous system (CNS) characterized by mononuclear cell infiltration, demyelination, and paralysis. We previously demonstrated a role for chemokines in acute and relapsing EAE pathogenesis. Presently, we investigated the role of CC chemokine receptor 2 (CCR2) in acute EAE. CCR2–/– mice did not develop clinical EAE or CNS histopathology, and showed a significant reduction in T cell– and CNS-infiltrating CD45highF4/80+ monocyte subpopulations. Peripheral lymphocytes from CCR2–/– mice produced comparable levels of interferon-gamma (IFN-{gamma}) and interleukin (IL)-2 in response to antigen-specific restimulation when compared with control mice. Adoptively transferred myelin oligodendrocyte glycoprotein 35-55–specific T cells lacking expression of CCR2 were able to induce EAE, whereas CCR2–/– recipients of wild-type T cells failed to develop disease. These results suggest that CCR2 expression on host-derived mononuclear cells is critical for disease induction.

Key Words: multiple sclerosis • experimental autoimmune encephalomyelitis • CC chemokine receptor 2 • knockout • CCL2

© 2000 The Rockefeller University Press


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