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To: scaram(o)uche who wrote (587)	9/7/2000 3:01:40 PM
From: PuddleGlum	Respond to of 3044

Joe's news was just confirmed: biz.yahoo.com

To: scaram(o)uche who wrote (587)	10/2/2000 7:20:42 PM
From: scaram(o)uche	Read Replies (3) \| Respond to of 3044

The Journal of Experimental Medicine, Volume 192, Number 7, October 2, 2000 1075-1080 Brief Definitive Report Resistance to Experimental Autoimmune Encephalomyelitis in Mice Lacking the CC Chemokine Receptor (CCR)2 Leonid Iziksona, Robyn S. Kleinb, Israel F. Charoc, Howard L. Weinera, and Andrew D. Lusterb a Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115 b Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy, and Immunology, Massachussetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114 c Gladstone Institute, University of California at San Francisco, San Francisco, California 94141 Correspondence to: Andrew D. Luster, Massachusetts General Hospital-East, Bldg. 149 13th St., Charlestown, MA 02129. Monocyte recruitment to the central nervous system (CNS) is a necessary step in the development of pathologic inflammatory lesions in experimental autoimmune encephalomyelitis (EAE), a murine model of multiple sclerosis. Monocyte chemoattractant protein (MCP)-1, a potent agonist for directed monocyte migration, has been implicated in the pathogenesis of EAE. Here we report that deficiency in CC chemokine receptor (CCR)2, the receptor for MCP-1, confers resistance to EAE induced with a peptide derived from myelin oligodendrocyte glycoprotein peptide 35–55 (MOGp35–55). CCR2-/- mice immunized with MOGp35–55 failed to develop mononuclear cell inflammatory infiltrates in the CNS and failed to increase CNS levels of the chemokines RANTES (regulated on activation, normal T cell expressed and secreted), MCP-1, and interferon (IFN)-inducible protein 10 (IP-10) as well the chemokine receptors CCR1, CCR2, and CCR5. Additionally, T cells from CCR2-/- immunized mice showed decreased antigen-induced proliferation and production of IFN- compared with wild-type immunized controls, suggesting that CCR2 enhances the T helper cell type 1 immune response in EAE. These data indicate that CCR2 plays a necessary and nonredundant role in the pathogenesis of EAE.