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Resistance to experimental autoimmune encephalomyelitis in mice lacking the CC chemokine receptor (CCR)2.
J Exp Med. 2000 Oct 02; 192(7):1075-80.JE

Abstract

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-gamma 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.

Authors+Show Affiliations

Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

11015448

Citation

Izikson, L, et al. "Resistance to Experimental Autoimmune Encephalomyelitis in Mice Lacking the CC Chemokine Receptor (CCR)2." The Journal of Experimental Medicine, vol. 192, no. 7, 2000, pp. 1075-80.
Izikson L, Klein RS, Charo IF, et al. Resistance to experimental autoimmune encephalomyelitis in mice lacking the CC chemokine receptor (CCR)2. J Exp Med. 2000;192(7):1075-80.
Izikson, L., Klein, R. S., Charo, I. F., Weiner, H. L., & Luster, A. D. (2000). Resistance to experimental autoimmune encephalomyelitis in mice lacking the CC chemokine receptor (CCR)2. The Journal of Experimental Medicine, 192(7), 1075-80.
Izikson L, et al. Resistance to Experimental Autoimmune Encephalomyelitis in Mice Lacking the CC Chemokine Receptor (CCR)2. J Exp Med. 2000 Oct 2;192(7):1075-80. PubMed PMID: 11015448.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Resistance to experimental autoimmune encephalomyelitis in mice lacking the CC chemokine receptor (CCR)2. AU - Izikson,L, AU - Klein,R S, AU - Charo,I F, AU - Weiner,H L, AU - Luster,A D, PY - 2000/10/4/pubmed PY - 2001/2/28/medline PY - 2000/10/4/entrez SP - 1075 EP - 80 JF - The Journal of experimental medicine JO - J Exp Med VL - 192 IS - 7 N2 - 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-gamma 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. SN - 0022-1007 UR - https://www.unboundmedicine.com/medline/citation/11015448/Resistance_to_experimental_autoimmune_encephalomyelitis_in_mice_lacking_the_CC_chemokine_receptor__CCR_2_ DB - PRIME DP - Unbound Medicine ER -