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dc.contributor.authorCueto, Francisco J. 
dc.contributor.authorSancho, David 
dc.date.accessioned2021-09-15T08:04:31Z
dc.date.available2021-09-15T08:04:31Z
dc.date.issued2021-03-26
dc.identifier.citationCancers (Basel). 2021; 13(7):1525es_ES
dc.identifier.issn2072-6694es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/13391
dc.description.abstractDendritic cells (DCs) prime anti-tumor T cell responses in tumor-draining lymph nodes and can restimulate T effector responses in the tumor site. Thus, in addition to unleashing T cell effector activity, current immunotherapies should be directed to boost DC function. Herein, we review the potential function of Flt3L as a tool for cancer immunotherapy. Flt3L is a growth factor that acts in Flt3-expressing multipotent progenitors and common lymphoid progenitors. Despite the broad expression of Flt3 in the hematopoietic progenitors, the main effect of the Flt3/Flt3L axis, revealed by the characterization of mice deficient in these genes, is the generation of conventional DCs (cDCs) and plasmacytoid DCs (pDCs). However, Flt3 signaling through PI3K and mTOR may also affect the function of mature DCs. We recapitulate the use of Flt3L in preclinical studies either as a single agent or in combination with other cancer therapies. We also analyze the use of Flt3L in clinical trials. The strong correlation between type 1 cDC (cDC1) infiltration of human cancers with overall survival in many cancer types suggests the potential use of Flt3L to boost expansion of this DC subset. However, this may need the combination of Flt3L with other immunomodulatory agents to boost cancer immunotherapy.es_ES
dc.description.sponsorshipWork in the D.S. laboratory is funded by the CNIC; by the European Research Council (ERC-2016-Consolidator Grant 725091); by Agencia Estatal de Investigación (PID2019-108157RB); by Comunidad de Madrid (B2017/BMD-3733 Immunothercan-CM); by Fondo Solidario Juntos (BancoSantander); and by Fundació La Marató de TV3 (201723). The CNIC is supported by the Instituto deSalud Carlos III (ISCIII), the MICINN and the Pro CNIC Foundation.es_ES
dc.language.isoenges_ES
dc.publisherMDPIes_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.titleThe Flt3L/Flt3 Axis in Dendritic Cell Biology and Cancer Immunotherapy.es_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID33810248es_ES
dc.format.volume13es_ES
dc.format.number7es_ES
dc.format.page1525es_ES
dc.identifier.doi10.3390/cancers13071525es_ES
dc.contributor.funderCentro Nacional de Investigaciones Cardiovasculares (España)
dc.contributor.funderComunidad de Madrid
dc.contributor.funderBanco Santander
dc.contributor.funderFundación La Mataró TV3
dc.contributor.funderInstituto de Salud Carlos III - ISCIII
dc.contributor.funderFundación ProCNIC
dc.contributor.funderMinisterio de Ciencia e Innovación (España)
dc.description.peerreviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.3390/cancers13071525es_ES
dc.identifier.journalCancerses_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Inmunobiologíaes_ES
dc.repisalud.institucionCNICes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/H2020/ERC-2016-725091es_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/PID2019-108157RBes_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/B2017/BMD-3733es_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/201723es_ES


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Atribución 4.0 Internacional
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