Mostrar el registro sencillo del ítem

dc.contributor.authordel Fresno, Carlos 
dc.contributor.authorSanz-Leal, Paula 
dc.contributor.authorEnamorado, Michel 
dc.contributor.authorWculek, Stefanie K 
dc.contributor.authorMartinez-Cano, Sarai 
dc.contributor.authorBlanco-Menendez, Noelia 
dc.contributor.authorSchulz, Oliver
dc.contributor.authorGallizioli, Mattia
dc.contributor.authorMiró-Mur, Francesc
dc.contributor.authorCano, Eva 
dc.contributor.authorPlanas, Anna
dc.contributor.authorSancho, David 
dc.date.accessioned2018-10-22T13:18:00Z
dc.date.available2018-10-22T13:18:00Z
dc.date.issued2018-10-19
dc.identifier.citationScience. 2018; 362(6412):351-356es_ES
dc.identifier.issn0036-8075es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/6502
dc.description.abstractHost 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.sponsorshipC.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.isoenges_ES
dc.publisherAmerican Association for the Advancement of Science (AAAS) es_ES
dc.type.hasVersionAMes_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.titleDNGR-1 in dendritic cells limits tissue damage by dampening neutrophil recruitmentes_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.identifier.pubmedID30337411es_ES
dc.format.volume362es_ES
dc.format.number6412es_ES
dc.format.page351-356es_ES
dc.identifier.doi10.1126/science.aan8423es_ES
dc.contributor.funderAsociación Española Contra el Cáncer 
dc.contributor.funderMinisterio de Ciencia, Innovación y Universidades (España) 
dc.contributor.funderEuropean Molecular Biology Organization 
dc.contributor.funderUnión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF) 
dc.contributor.funderComunidad de Madrid (España) 
dc.contributor.funderInstituto de Salud Carlos III 
dc.contributor.funderFundación La Marató TV3 
dc.contributor.funderUnión Europea. Comisión Europea 
dc.contributor.funderUnión Europea. Comisión Europea. European Research Council (ERC) 
dc.contributor.funderFundación ProCNIC 
dc.description.peerreviewedes_ES
dc.identifier.e-issn1095-9203es_ES
dc.relation.publisherversionhttps://doi.org/10.1126/science.aan8423es_ES
dc.identifier.journalSciencees_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Inmunobiologíaes_ES
dc.repisalud.institucionCNICes_ES
dc.relation.projectIDMINECO/ICTI2013-2016/SAF2016-79040-Res_ES
dc.relation.projectIDMINECO/ICTI2013-2016/BES-2015-072699es_ES
dc.relation.projectIDMINECO/ICTI2013-2016/SEV-2015-0505es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/H2020/635122es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/H2020/725091es_ES
dc.rights.accessRightsopen accesses_ES


Ficheros en el ítem

Acceso Abierto
Thumbnail
Acceso Abierto
Thumbnail

Este ítem aparece en la(s) siguiente(s) colección(ones)

Mostrar el registro sencillo del ítem

Atribución-NoComercial-CompartirIgual 4.0 Internacional
Este Item está sujeto a una licencia Creative Commons: Atribución-NoComercial-CompartirIgual 4.0 Internacional