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dc.contributor.author | Cueto, Francisco J. | |
dc.contributor.author | del Fresno, Carlos | |
dc.contributor.author | Sancho, David | |
dc.date.accessioned | 2020-04-03T10:42:16Z | |
dc.date.available | 2020-04-03T10:42:16Z | |
dc.date.issued | 2019-03 | |
dc.identifier.citation | Front Immunol. 2020; 10:3146 | es_ES |
dc.identifier.issn | 1664-3224 | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/9440 | |
dc.description.abstract | DNGR-1 (encoded by CLEC9A) is a C-type lectin receptor (CLR) with an expression profile that is mainly restricted to type 1 conventional dendritic cells (cDC1s) both in mice and humans. This delimited expression pattern makes it appropriate for defining a cDC1 signature and for therapeutic targeting of this population, promoting immunity in mouse models. Functionally, DNGR-1 binds F-actin, which is confined within the intracellular space in healthy cells, but is exposed when plasma membrane integrity is compromised, as happens in necrosis. Upon F-actin binding, DNGR-1 signals through SYK and mediates cross-presentation of dead cell-associated antigens. Cross-presentation to CD8+ T cells promoted by DNGR-1 during viral infections is key for cross-priming tissue-resident memory precursors in the lymph node. However, in contrast to other closely related CLRs such as Dectin-1, DNGR-1 does not activate NFκB. Instead, recent findings show that DNGR-1 can activate SHP-1 to limit inflammation triggered by heterologous receptors, which results in reduced production of inflammatory chemokines and neutrophil recruitment into damaged tissues in both sterile and infectious processes. Hence, DNGR-1 reduces immunopathology associated with tissue damage, promoting disease tolerance to safeguard tissue integrity. How DNGR-1 signals are conditioned by the microenvironment and the detailed molecular mechanisms underlying DNGR-1 function have not been elucidated. Here, we review the expression pattern and structural features of DNGR-1, and the biological relevance of the detection of tissue damage through this CLR. | es_ES |
dc.description.sponsorship | FC was a recipient of a PhD La Caixa fellowship (LCF/BQ/ES14/10320011). CF was supported by AECC Foundation (INVES192DELF). Work in the DS laboratory was funded by the CNIC; by the European Research Council (ERC-2016-Consolidator Grant 725091); by the European Commission (635122-PROCROP H2020); by Ministerio de Ciencia, Innovación e Universidades (MICINN), Agencia Estatal de Investigación and Fondo Europeo de Desarrollo Regional (FEDER) (SAF2016-79040-R); by Comunidad de Madrid (B2017/BMD-3733 Immunothercan-CM); by FIS-Instituto de Salud Carlos III, MICINN and FEDER (RD16/0015/0018-REEM); by Acteria Foundation; by Atresmedia (Constantes y Vitales prize); and by Fundació La Marató de TV3 (201723). The CNIC was supported by the Instituto de Salud Carlos III (ISCIII), the MICINN, and the Pro CNIC Foundation, and is a Severo Ochoa Center of Excellence (SEV-2015-0505). | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Frontiers Media | es_ES |
dc.type.hasVersion | VoR | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | * |
dc.subject | C-type lectin receptor | es_ES |
dc.subject | Clec9a | es_ES |
dc.subject | DNGR-1 | es_ES |
dc.subject | Cross-presentation | es_ES |
dc.subject | Dendritic cells | es_ES |
dc.subject | Immunity | es_ES |
dc.subject | Inflammation | es_ES |
dc.title | DNGR-1, a Dendritic Cell-Specific Sensor of Tissue Damage That Dually Modulates Immunity and Inflammation | es_ES |
dc.type | journal article | es_ES |
dc.rights.license | Atribución 4.0 Internacional | * |
dc.identifier.pubmedID | 32117205 | es_ES |
dc.format.volume | 10 | es_ES |
dc.format.page | 3146 | es_ES |
dc.identifier.doi | 10.3389/fimmu.2019.03146 | es_ES |
dc.contributor.funder | Asociación Española Contra el Cáncer | |
dc.contributor.funder | Fundación La Caixa | |
dc.contributor.funder | Fundación ProCNIC | |
dc.contributor.funder | Unión Europea. Comisión Europea | |
dc.contributor.funder | European Research Council | |
dc.contributor.funder | Ministerio de Ciencia, Innovación y Universidades (España) | |
dc.contributor.funder | European Regional Development Fund | |
dc.contributor.funder | Comunidad de Madrid (España) | |
dc.contributor.funder | Instituto de Salud Carlos III | |
dc.contributor.funder | Fundación La Marató TV3 | |
dc.contributor.funder | Fondation ACTERIA (Acting on European Research in Immunology and Allergology) | |
dc.contributor.funder | Atresmedia | |
dc.description.peerreviewed | Sí | es_ES |
dc.identifier.e-issn | 1664-3224 | es_ES |
dc.relation.publisherversion | https://doi.org/10.3389/fimmu.2019.03146 | es_ES |
dc.identifier.journal | Frontiers in immunology | es_ES |
dc.repisalud.orgCNIC | CNIC::Grupos de investigación::Inmunobiología | es_ES |
dc.repisalud.institucion | CNIC | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/SEV-2015-0505 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/EC/H2020/725091 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/EC/H2020/635122 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/SAF2016-79040-R | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/B2017/BMD-3733 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/RD16/0015/0018-REEM | es_ES |
dc.rights.accessRights | open access | es_ES |