CD200R1 Agonist Attenuates Mechanisms of Chronic Disease in a Murine Model of Multiple Sclerosis

• DOI: 10.1523/jneurosci.4272-09.2010
• Publication Date: 2010-02-10T17:33:24Z
• Authors: Yingru Liu; Yoshio Bando; David Vargas-Lowy; Wassim Elyaman; Samia J. Khoury; Tao Huang; Karin Reif; Tanuja Chitnis
• Keywords: Myelin oligodendrocyte glycoprotein; Proinflammatory cytokine

To assess the effects and mechanisms of a CD200R1 agonist administered during progressive stage multiple sclerosis model, we (CD200Fc) or control IgG2a chronic phase disease (days 10–30) in mice with experimental autoimmune encephalomyelitis (EAE), induced using myelin oligodendrocyte glycoprotein peptide 35–55 (MOG35–55) peptide. We found that administration CD200Fc stages EAE reduced severity, demyelination, axonal damage, through modulation several key mechanisms. treatment suppressed macrophage microglial accumulation within CNS, part downregulation adhesion molecules VLA-4 LFA-1, which are necessary for migration. Additionally, expression activation markers MHC-II CD80 production proinflammatory cytokines IL-6, tumor necrosis factor-α, nitric oxide by CD11b + cells were decreased both spleen CNS CD200Fc-treated animals. Antigen-presenting cell function was mice, but there no significant alterations on T phenotype. increased apoptosis not astrocytes. In contrast, addition protected oligodendrocytes from vitro vivo . Our results demonstrate agonists modulate myeloid- non-myeloid-related model may be effective other neurodegenerative diseases.