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dc.contributor.author | Carrillo-Salinas, F. J. | - |
dc.contributor.author | Navarrete, Carmen | - |
dc.contributor.author | Mecha, Miriam | - |
dc.contributor.author | Feliú, Ana | - |
dc.contributor.author | Collado, J.A. | - |
dc.contributor.author | Cantarero, Irene | - |
dc.contributor.author | Bellido, María Luz | - |
dc.contributor.author | Muñoz, E. | - |
dc.contributor.author | Guaza, Carmen | - |
dc.date.accessioned | 2017-10-18T11:21:38Z | - |
dc.date.available | 2017-10-18T11:21:38Z | - |
dc.date.issued | 2014 | - |
dc.identifier | doi: 10.1371/journal.pone.0094733 | - |
dc.identifier | issn: 1932-6203 | - |
dc.identifier.citation | PLoS ONE 9 (2014) | - |
dc.identifier.uri | http://hdl.handle.net/10261/156411 | - |
dc.description.abstract | Phytocannabinoids that do not produce psychotropic effects are considered of special interest as novel therapeutic agents in CNS diseases. A cannabigerol quinone, the compound VCE-003, has been shown to alleviate symptoms in a viral model of multiple sclerosis (MS). Hence, we studied T cells and macrophages as targets for VCE-003 and its efficacy in an autoimmune model of MS. Proliferation, cell cycle, expression of activation markers was assessed by FACs in human primary T cells, and cytokine and chemokine production was evaluated. Transcription was studied in Jurkat cells and RAW264.7 cells were used to study the effects of VCE-003 on IL-17-induced macrophage polarization to a M1 phenotype. Experimental autoimmune encephalomyelitis (EAE) was induced by myelin oligodendrocyte glycoprotein (MOG35-55) immunization and spinal cord pathology was assessed by immunohistochemistry. Neurological impairment was evaluated using disease scores. We show here that VCE-003 inhibits CD3/CD28-induced proliferation, cell cycle progression and the expression of the IL-2Ra and ICAM-1 activation markers in human primary T cells. VCE-003 inhibits the secretion of Th1/Th17 cytokines and chemokines in primary murine T cells, and it reduces the transcriptional activity of the IL-2, IL-17 and TNFa promoters induced by CD3/ CD28. In addition, VCE-003 and JWH-133, a selective CB2 agonist, dampened the IL-17-induced polarization of macrophages to a pro-inflammatory M1 profile. VCE-003 also prevented LPS-induced iNOS expression in microglia. VCE-003 ameliorates the neurological defects and the severity of MOG-induced EAE in mice through CB2 and PPARc receptor activation. A reduction in cell infiltrates, mainly CD4T cells, was observed, and Th1 and Th17 responses were inhibited in the spinal cord of VCE-003-treated mice, accompanied by weaker microglial activation, structural preservation of myelin sheets and reduced axonal damage. This study highlights the therapeutic potential of VCE-003 as an agent for the treatment of human immune diseases with both inflammatory and autoimmune components. © 2014 Carrillo-Salinas et al. | - |
dc.publisher | Public Library of Science | - |
dc.relation.isversionof | Publisher's version | - |
dc.rights | openAccess | - |
dc.subject | Experimental autoimmune | - |
dc.title | A cannabigerol derivative suppresses immune responses and protects mice from experimental autoimmune encephalomyelitis | - |
dc.type | artículo | - |
dc.identifier.doi | 10.1371/journal.pone.0094733 | - |
dc.date.updated | 2017-10-18T11:21:39Z | - |
dc.description.version | Peer Reviewed | - |
dc.language.rfc3066 | eng | - |
dc.relation.csic | Sí | - |
dc.identifier.pmid | 24727978 | - |
dc.type.coar | http://purl.org/coar/resource_type/c_6501 | es_ES |
item.openairetype | artículo | - |
item.cerifentitytype | Publications | - |
item.grantfulltext | open | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.fulltext | With Fulltext | - |
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