期刊
JOURNAL OF NEUROIMMUNOLOGY
卷 194, 期 1-2, 页码 62-69出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jneuroim.2007.11.013
关键词
CD200; CD200-receptor; myeloid cells; experimental autoimmune encephalomyelitis; multiple sclerosis; inflammation
Multiple sclerosis is a chronic disabling CNS disorder, characterized by autoimmune inflammatory demyelination and neurodegeneration. CD200, broadly expressed on neurons and endothelial cells, mediates inhibitory signals through its receptor, CD200R, on cells of myeloid origin. Antibody-mediated blockade of CD200R leads to an aggravated clinical course of rodent experimental autoimmune encephalomyelitis in vivo, accompanied by profoundly augmented cellular infiltrates consisting of T cells and activated iNOS(+) macrophages in inflammatory spinal cord lesions. In vitro blockade of CD200R on macrophages leads to enhanced IFN-gamma-induced release of IL6 and neuronal cell death in co-cultures with hippocampal neurons expressing CD200. CD200 and its receptor could also be detected on neurons and macrophages in human MS plaques. Therefore the CD200-CD200R pathway seems of critical relevance for macrophage-mediated damage in autoimmune inflammation of the CNS. (C) 2007 Elsevier B.V. All rights reserved.
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