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dc.contributor.author | del Fresno, Carlos | |
dc.contributor.author | Sanz-Leal, Paula | |
dc.contributor.author | Enamorado, Michel | |
dc.contributor.author | Wculek, Stefanie K | |
dc.contributor.author | Martinez-Cano, Sarai | |
dc.contributor.author | Blanco-Menendez, Noelia | |
dc.contributor.author | Schulz, Oliver | |
dc.contributor.author | Gallizioli, Mattia | |
dc.contributor.author | Miró-Mur, Francesc | |
dc.contributor.author | Cano, Eva | |
dc.contributor.author | Planas, Anna | |
dc.contributor.author | Sancho, David | |
dc.date.accessioned | 2018-10-22T13:18:00Z | |
dc.date.available | 2018-10-22T13:18:00Z | |
dc.date.issued | 2018-10-19 | |
dc.identifier.citation | Science. 2018; 362(6412):351-356 | es_ES |
dc.identifier.issn | 0036-8075 | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/6502 | |
dc.description.abstract | Host injury triggers feedback mechanisms that limit tissue damage. Conventional type 1 dendritic cells (cDC1s) express dendritic cell natural killer lectin group receptor-1 (DNGR-1), encoded by the gene Clec9a, which senses tissue damage and favors cross-presentation of dead-cell material to CD8+ T cells. Here we find that DNGR-1 additionally reduces host-damaging inflammatory responses induced by sterile and infectious tissue injury in mice. DNGR-1 deficiency leads to exacerbated caerulein-induced necrotizing pancreatitis and increased pathology during systemic Candida albicans infection without affecting fungal burden. This effect is B and T cell-independent and attributable to increased neutrophilia in DNGR-1-deficient settings. Mechanistically, DNGR-1 engagement activates SHP-1 and inhibits MIP-2 (encoded by Cxcl2) production by cDC1s during Candida infection. This consequently restrains neutrophil recruitment and promotes disease tolerance. Thus, DNGR-1-mediated sensing of injury by cDC1s serves as a rheostat for the control of tissue damage, innate immunity, and immunopathology. | es_ES |
dc.description.sponsorship | C.d.F. is supported by AECC Foundation as recipient of an “Ayuda Fundación Científica AECC a personal investigador en cancer”. P.S.L. is funded by grant BES-2015- 072699 from Spanish Ministerio de Ciencia, Innovación y Universidades (MCIU). M.E. is the recipient of a CNIC International PhD Programme fellowship “la Caixa”-Severo Ochoa OSLCCNIC- 2013-04. S.K.W. is supported by a European Molecular Biology Organization (EMBO) Long-term Fellowship (grant ALTF 438-2016) and a CNIC-International Postdoctoral Programme Fellowship (grant 17230-2016). Work in the D.S. laboratory is funded by the CNIC and grant SAF2016-79040-R from MCIU, Agencia Estatal de Investigación and Fondos Europeos de Desarrollo Regional (FEDER); B2017/BMD-3733 Immunothercan-CM from Comunidad de Madrid; RD16/0015/0018-REEM from FIS-Instituto de Salud Carlos III, MICINN and FEDER; Acteria Foundation; Constantes y Vitales prize (Atresmedia); La Marató de TV3 Foundation (201723); the European Commission (635122-PROCROP H2020) and the European Research Council (ERC-2016-Consolidator Grant 725091). The CNIC is supported by the MCIU 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 | American Association for the Advancement of Science (AAAS) | es_ES |
dc.type.hasVersion | AM | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-sa/4.0/ | * |
dc.title | DNGR-1 in dendritic cells limits tissue damage by dampening neutrophil recruitment | es_ES |
dc.type | journal article | es_ES |
dc.rights.license | Atribución-NoComercial-CompartirIgual 4.0 Internacional | * |
dc.identifier.pubmedID | 30337411 | es_ES |
dc.format.volume | 362 | es_ES |
dc.format.number | 6412 | es_ES |
dc.format.page | 351-356 | es_ES |
dc.identifier.doi | 10.1126/science.aan8423 | es_ES |
dc.contributor.funder | Asociación Española Contra el Cáncer | |
dc.contributor.funder | Ministerio de Ciencia, Innovación y Universidades (España) | |
dc.contributor.funder | European Molecular Biology Organization | |
dc.contributor.funder | Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF) | |
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 | Unión Europea. Comisión Europea | |
dc.contributor.funder | Unión Europea. Comisión Europea. European Research Council (ERC) | |
dc.contributor.funder | Fundación ProCNIC | |
dc.description.peerreviewed | Sí | es_ES |
dc.identifier.e-issn | 1095-9203 | es_ES |
dc.relation.publisherversion | https://doi.org/10.1126/science.aan8423 | es_ES |
dc.identifier.journal | Science | es_ES |
dc.repisalud.orgCNIC | CNIC::Grupos de investigación::Inmunobiología | es_ES |
dc.repisalud.institucion | CNIC | es_ES |
dc.relation.projectID | MINECO/ICTI2013-2016/SAF2016-79040-R | es_ES |
dc.relation.projectID | MINECO/ICTI2013-2016/BES-2015-072699 | es_ES |
dc.relation.projectID | MINECO/ICTI2013-2016/SEV-2015-0505 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/EC/H2020/635122 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/EC/H2020/725091 | es_ES |
dc.rights.accessRights | open access | es_ES |