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dc.contributor.authorBustos-Morán, Eugenio
dc.contributor.authorBlas-Rus, Noelia 
dc.contributor.authorAlcaraz-Serna, Ana
dc.contributor.authorIborra, Salvador 
dc.contributor.authorGonzález-Martínez, José
dc.contributor.authorMalumbres Martinez, Marcos 
dc.contributor.authorSanchez-Madrid, Francisco 
dc.date.accessioned2019-02-21T15:00:39Z
dc.date.available2019-02-21T15:00:39Z
dc.date.issued2019-02-18
dc.identifier.citationSci Rep. 2019; 9(1):2211es_ES
dc.identifier.issn2045-2322es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/7212
dc.description.abstractAurora A is a serine/threonine kinase whose role in cell cycle progression and tumour generation has been widely studied. Recent work has revealed an unexpected function for Aurora A during CD4+ T cell activation and, also, in graft versus host disease development. However, it remains unknown whether Aurora A is involved in CD8+ T cell effector function and in cytotoxic T lymphocyte-mediated antiviral response. Here, we show that Aurora A chemical inhibition leads to an impairment of both the peptide-specific cytotoxicity and the degranulation activity of CD8+ T cells. This finding was similarly proven for both mice and human CD8+ CTL activity. As a result of Aurora A blockade, we detected a reduction in the expression induced by T cell activation of genes classically related to the effector function of cytotoxic T lymphocytes such as granzyme B or perforin1. Finally, we have found that Aurora A is necessary for CD8+ T cell-mediated antiviral response, in an in vivo model of vaccinia virus infection. Thus, we can conclude that Aurora A activity is, indeed, needed for the proper effector function of cytotoxic T lymphocytes and for their activity against viral threats.es_ES
dc.description.sponsorshipThis study was supported by grants SAF2017/82886-R and BIO2012-37926 from the Spanish Ministry of Economy and Competitiveness, INFLAMUNE-CAMS2017/BMD-3671 from the Comunidad de Madrid and ERC-2011-AdG 294340-GENTRIS. Red Cardiovascular RD 12-0042-0056 from Instituto Salud Carlos III (ISCIII) and also CIBER Cardiovascular. The CNIC is supported by the Ministerio de Ciencia, Innovación y Universidades and the Pro CNIC Foundation, and it is a Severo Ochoa Centre of Excellence (SEV-2015-0505).es_ES
dc.language.isoenges_ES
dc.publisherNature Publishing Group es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.titleAurora A controls CD8+ T cell cytotoxic activity and antiviral responsees_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID30778113es_ES
dc.format.volume9es_ES
dc.format.number1es_ES
dc.format.page2211es_ES
dc.identifier.doi10.1038/s41598-019-38647-yes_ES
dc.contributor.funderMinisterio de Economía, Industria y Competitividad (España) 
dc.contributor.funderComunidad de Madrid (España) 
dc.contributor.funderInstituto de Salud Carlos III 
dc.contributor.funderMinisterio de Ciencia, Innovación y Universidades (España) 
dc.contributor.funderFundación ProCNIC 
dc.contributor.funderCentro de Investigación Biomedica en Red - CIBER
dc.contributor.funderUnión Europea. Comisión Europea 
dc.contributor.funderUnión Europea. Comisión Europea. European Research Council (ERC) 
dc.description.peerreviewedes_ES
dc.identifier.e-issn2045-2322es_ES
dc.relation.publisherversionhttps://doi.org/10.1038/s41598-019-38647-yes_ES
dc.identifier.journalScientific reportses_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Comunicación Intercelular en la Respuesta Inflamatoriaes_ES
dc.repisalud.institucionCNICes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/FP7/294340/EUes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2017/82886-Res_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/BIO2012-37926es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RD12-0042-0056es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SEV-2015-0505es_ES
dc.rights.accessRightsopen accesses_ES


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Atribución 4.0 Internacional
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