Show simple item record

dc.contributor.authorIborra, Salvador 
dc.contributor.authorIzquierdo-Fernandez, Helena Maria 
dc.contributor.authorMartinez-Lopez, Maria 
dc.contributor.authorBlanco-Menendez, Noelia 
dc.contributor.authorReis e Sousa, Caetano
dc.contributor.authorSancho, David
dc.identifier.citationJ Clin Invest. 2012; 122(5):1628-43es_ES
dc.description.abstractIn order to prime T cells, DCs integrate signals emanating directly from pathogens and from their noxious action on the host. DNGR-1 (CLEC9A) is a DC-restricted receptor that detects dead cells. Therefore, we investigated the possibility that DNGR-1 affects immunity to cytopathic viruses. DNGR-1 was essential for cross-presentation of dying vaccinia virus-infected (VACV-infected) cells to CD8(+) T cells in vitro. Following injection of VACV or VACV-infected cells into mice, DNGR-1 detected the ligand in dying infected cells and mediated cross-priming of anti-VACV CD8(+) T cells. Loss of DNGR-1 impaired the CD8+ cytotoxic response to VACV, especially against those virus strains that are most dependent on cross-presentation. The decrease in total anti-VACV CTL activity was associated with a profound increase in viral load and delayed resolution of the primary lesion. In addition, lack of DNGR-1 markedly diminished protection from infection induced by vaccination with the modified vaccinia Ankara (MVA) strain. DNGR-1 thus contributes to anti-VACV immunity, following both primary infection and vaccination. The non-redundant ability of DNGR-1 to regulate cross-presentation of viral antigens suggests that this form of regulation of antiviral immunity could be exploited for vaccination.es_ES
dc.description.sponsorshipWork in D. Sancho’s laboratory is funded by the CNIC and grants from the Spanish Ministry of Science and Innovation (SAF-2010-15120) and the European Research Council (ERC Starting Independent Researcher Grant 2010, ERC-2010-StG 260414). D. Sancho is the recipient of a Ramón y Cajal fellowship (RYC-2009-04235) from the Spanish Ministry of Science and Innovation.es_ES
dc.publisherAmerican Society for Clinical Investigation (ASCI) es_ES
dc.subject.meshAdaptive Immunity es_ES
dc.subject.meshAnimals es_ES
dc.subject.meshAntigen Presentation es_ES
dc.subject.meshAntigens, Viral es_ES
dc.subject.meshApoptosis es_ES
dc.subject.meshCD8-Positive T-Lymphocytes es_ES
dc.subject.meshCells, Cultured es_ES
dc.subject.meshDendritic Cells es_ES
dc.subject.meshGene Knockout Techniques es_ES
dc.subject.meshInterferon-gamma es_ES
dc.subject.meshIntracellular Signaling Peptides and Proteins es_ES
dc.subject.meshLectins, C-Type es_ES
dc.subject.meshLysosomes es_ES
dc.subject.meshMice es_ES
dc.subject.meshMice, Inbred C57BL es_ES
dc.subject.meshMice, Transgenic es_ES
dc.subject.meshNecrosis es_ES
dc.subject.meshProtein-Tyrosine Kinases es_ES
dc.subject.meshReceptors, Immunologic es_ES
dc.subject.meshSyk Kinase es_ES
dc.subject.meshVaccinia es_ES
dc.subject.meshVaccinia virus es_ES
dc.subject.meshViral Load es_ES
dc.subject.meshCross-Priming es_ES
dc.titleThe DC receptor DNGR-1 mediates cross-priming of CTLs during vaccinia virus infection in micees_ES
dc.typejournal articlees_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.contributor.funderMinisterio de Ciencia e Innovación (España)
dc.contributor.funderEuropean Research Council
dc.identifier.journalThe Journal of clinical investigationes_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Inmunobiologíaes_ES
dc.rights.accessRightsopen accesses_ES

Files in this item

Acceso Abierto

This item appears in the following Collection(s)

Show simple item record

Attribution-NonCommercial-NoDerivatives 4.0 Internacional
This item is licensed under a: Attribution-NonCommercial-NoDerivatives 4.0 Internacional