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Title

CD200-CD200R1 interaction contributes to neuroprotective effects of anandamide on experimentally induced inflammation

AuthorsHernangómez-Herrero, Miriam ; Mestre, Leyre ; Correa, Fernando Gabriel ; Loría, Frida ; Mecha, Miriam ; Ínigo, Paula M.; Docagne, Fabian ; Williams, R. O.; Borrell, José ; Guaza, Carmen
Issue DateSep-2012
PublisherJohn Wiley & Sons
CitationGlia 60(9): 1437-1450 (2012)
AbstractThe endocannabinoid anandamide (AEA) is released by macrophages and microglia on pathological neuroinflammatory conditions such as multiple sclerosis (MS). CD200 is a membrane glycoprotein expressed in neurons that suppresses immune activity via its receptor (CD200R) mainly located in macrophages/microglia. CD200-CD200R interactions contribute to the brain immune privileged status. In this study, we show that AEA protects neurons from microglia-induced neurotoxicity via CD200-CD200R interaction. AEA increases the expression of CD200R1 in LPS/IFN-γ activated microglia through the activation of CB 2 receptors. The neuroprotective effect of AEA disappears when microglial cells derive from CD200R1 -/- mice. We also show that engagement of CD200R1 by CD200Fc decreased the production of the proinflammatory cytokines IL-1β and IL-6, but increased IL-10 in activated microglia. In the chronic phases of Theiler's virus-induced demyelinating disease (TMEV-IDD) the expression of CD200 and CD200R1 was reduced in the spinal cord. AEA-treated animals up-regulated the expression of CD200 and CD200R1, restoring levels found in sham animals together with increased expression of IL-10 and reduced expression of IL-1β and IL-6. Treated animals also improved their motor behavior. Because AEA up-regulated the expression of CD200R1 in microglia, but failed to enhance CD200 in neurons we suggest that AEA-induced up-regulation of CD200 in TMEV-IDD is likely due to IL-10 as this cytokine increases CD200 in neurons. Our findings provide a new mechanism of action of AEA to limit immune response in the inflamed brain. © 2012 Wiley Periodicals, Inc.
URIhttp://hdl.handle.net/10261/60358
DOI10.1002/glia.22366
Identifiersdoi: 10.1002/glia.22366
issn: 0894-1491
Appears in Collections:(IC) Artículos
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