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CNS inflammation and neuronal degeneration is aggravated by impaired CD200-CD200R-mediated macrophage silencing.

Authors: Meuth, Sven G  Simon, Ole J  Grimm, Alexander  Melzer, Nico  Herrmann, Alexander M  Spitzer, Philipp  Landgraf, Peter  Wiendl, Heinz 
Citation: Meuth SG, etal., J Neuroimmunol. 2008 Feb;194(1-2):62-9. doi: 10.1016/j.jneuroim.2007.11.013.
Pubmed: (View Article at PubMed) PMID:18164423
DOI: Full-text: DOI:10.1016/j.jneuroim.2007.11.013

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.


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CRRD Object Information
CRRD ID: 13792521
Created: 2018-09-12
Species: All species
Last Modified: 2018-09-12
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.