Experimental Autoimmune Encephalomyelitis: CC Chemokine Receptor Expression by Trafficking Cells

2002 ◽  
Vol 19 (4) ◽  
pp. 175-181 ◽  
Author(s):  
Andrzej R. Glabinski ◽  
Bartosz Bielecki ◽  
Sage O'Bryant ◽  
Krzysztof Selmaj ◽  
Richard M. Ransohoff
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Chemokine Receptor ◽  
Receptor Expression ◽  
Autoimmune Encephalomyelitis ◽  
Chemokine Receptor Expression ◽  
Cc Chemokine ◽  
Experimental Autoimmune

scholarly journals Resistance to Experimental Autoimmune Encephalomyelitis in Mice Lacking the Cc Chemokine Receptor (Ccr2)

2000 ◽  
Vol 192 (7) ◽  
pp. 1075-1080 ◽  
Author(s):  
Leonid Izikson ◽  
Robyn S. Klein ◽  
Israel F. Charo ◽  
Howard L. Weiner ◽  
Andrew D. Luster
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Chemokine Receptor ◽  
Chemokine Receptors ◽  
Autoimmune Encephalomyelitis ◽  
Cc Chemokine ◽  
Monocyte Migration ◽  
Helper Cell Type ◽  
Inducible Protein ◽  
Inflammatory Infiltrates ◽  
Experimental Autoimmune

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-γ 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.

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

2000 ◽  
Vol 192 (6) ◽  
pp. 899-906 ◽  
Author(s):  
Brian T. Fife ◽  
Gary B. Huffnagle ◽  
William A. Kuziel ◽  
William J. Karpus
Keyword(s):  
T Cells ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Chemokine Receptor ◽  
Mononuclear Cells ◽  
Autoimmune Encephalomyelitis ◽  
Cc Chemokine ◽  
Ccr2 Expression ◽  
Cc Chemokine Receptor 2 ◽  
The Central Nervous System ◽  
Experimental Autoimmune

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-γ) 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.

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