CXC Chemokine Receptors Expression during Chronic Relapsing Experimental Autoimmune Encephalomyelitis

2006 ◽  
Vol 917 (1) ◽  
pp. 135-144 ◽  
Author(s):  
ANDRZEJ R. GLABINSKI ◽  
SAGE O'BRYANT ◽  
KRZYSZTOF SELMAJ ◽  
RICHARD M. RANSOHOFF
2006 ◽  
Vol 176 (12) ◽  
pp. 7676-7685 ◽  
Author(s):  
Ludmila V. Bagaeva ◽  
Praveen Rao ◽  
James M. Powers ◽  
Benjamin M. Segal

2000 ◽  
Vol 192 (7) ◽  
pp. 1075-1080 ◽  
Author(s):  
Leonid Izikson ◽  
Robyn S. Klein ◽  
Israel F. Charo ◽  
Howard L. Weiner ◽  
Andrew D. Luster

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.


2008 ◽  
Vol 0 (0) ◽  
pp. 080415182616831-??? ◽  
Author(s):  
Rachel E. Kohler ◽  
Iain Comerford ◽  
Scott Townley ◽  
Sarah Haylock-Jacobs ◽  
Ian Clark-Lewis ◽  
...  

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