Detrimental contribution of the immuno-inhibitor B7-H1 to rabies virus encephalitis

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dc.contributor.authorLafon, Monique
dc.contributor.authorMégret, Françoise
dc.contributor.authorMeuth, Sven G.
dc.contributor.authorSimon, Ole
dc.contributor.authorVelandia-Romero, Myriam Lucía
dc.contributor.authorLafage, Mireille
dc.contributor.authorChen, Lieping
dc.contributor.authorAlexopoulou, Lena
dc.contributor.authorFlavell, Richard A.
dc.contributor.authorPrehaud, Prehaud
dc.contributor.authorWiendl, Heinz
dc.contributor.orcidVelandia-Romero, Myriam Lucía [0000-0002-3340-7304]
dc.date.accessioned2020-08-31T11:19:22Z
dc.date.available2020-08-31T11:19:22Z
dc.date.issued2008
dc.description.abstractenglishRabies virus is the etiological agent of an acute encephalitis, which in absence of post exposure treatment is fatal in almost all cases. Virus lethality rests on its ability to evade the immune response. In this study, we analyzed the role of the immuno-inhibitory molecule B7-H1 in this virus strategy. We showed that in the brain and spinal cord of mice, rabies virus infection resulted in significant up-regulation of B7-H1 expression, which is specifically expressed in infected neurons. Correlatively, clinical rabies in B7-H1−/− mice is markedly less severe than in wild-type mice. B7-H1−/− mice display resistance to rabies. Virus invasion is reduced and the level of migratory CD8 T cells increases into the nervous system, while CD4/CD8 ratio remains unchanged in the periphery. In vivo, neuronal B7-H1 expression is critically depending on TLR3 signaling and IFN-β, because TLR3−/− mice—in which IFN-β production is reduced—showed only a limited increase of B7-H1 transcripts after infection. These data provide evidence that neurons can express the B7-H1 molecule after viral stress or exposure to a particular cytokine environment. They show that the B7-H1/PD-1 pathway can be exploited locally and in an organ specific manner—here the nervous system—by a neurotropic virus to promote successful host invasion.eng
dc.format.mimetypeapplication/pdf
dc.identifier.doihttps://doi.org/10.4049/jimmunol.180.11.7506
dc.identifier.instnameinstname:Universidad El Bosquespa
dc.identifier.issn1550-6606
dc.identifier.reponamereponame:Repositorio Institucional Universidad El Bosquespa
dc.identifier.repourlhttps://repositorio.unbosque.edu.co
dc.identifier.urihttps://hdl.handle.net/20.500.12495/3894
dc.language.isoeng
dc.publisherThe American Association of Immunologistsspa
dc.publisher.journalThe Journal of Immunologyspa
dc.relation.ispartofseriesThe Journal of Immunology, 1550-6606, Vol. 180, Nro. 11, 2008 p. 7506-7515spa
dc.relation.urihttps://www.jimmunol.org/content/180/11/7506.long
dc.rights.accessrightshttps://purl.org/coar/access_right/c_abf2
dc.rights.accessrightsinfo:eu-repo/semantics/openAccess
dc.rights.accessrightsAcceso abierto
dc.rights.creativecommons2008-06
dc.rights.localAcceso abiertospa
dc.subject.decsVirus de la rabiaspa
dc.subject.decsVirus ARNspa
dc.subject.decsVirus de la encefalitisspa
dc.titleDetrimental contribution of the immuno-inhibitor B7-H1 to rabies virus encephalitisspa
dc.title.translatedDetrimental contribution of the immuno-inhibitor B7-H1 to rabies virus encephalitisspa
dc.type.coarhttps://purl.org/coar/resource_type/c_6501
dc.type.driverinfo:eu-repo/semantics/article
dc.type.hasversioninfo:eu-repo/semantics/publishedVersion
dc.type.localArtículo de revista

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