dc.contributor.author | Cueto, Francisco J. | |
dc.contributor.author | Sancho, David | |
dc.date.accessioned | 2021-09-15T08:04:31Z | |
dc.date.available | 2021-09-15T08:04:31Z | |
dc.date.issued | 2021-03-26 | |
dc.identifier.citation | Cancers (Basel). 2021; 13(7):1525 | es_ES |
dc.identifier.issn | 2072-6694 | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/13391 | |
dc.description.abstract | Dendritic 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.sponsorship | Work 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.iso | eng | es_ES |
dc.publisher | Multidisciplinary Digital Publishing Institute (MDPI) | es_ES |
dc.type.hasVersion | VoR | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | * |
dc.title | The Flt3L/Flt3 Axis in Dendritic Cell Biology and Cancer Immunotherapy. | es_ES |
dc.type | journal article | es_ES |
dc.rights.license | Atribución 4.0 Internacional | * |
dc.identifier.pubmedID | 33810248 | es_ES |
dc.format.volume | 13 | es_ES |
dc.format.number | 7 | es_ES |
dc.format.page | 1525 | es_ES |
dc.identifier.doi | 10.3390/cancers13071525 | es_ES |
dc.contributor.funder | Centro Nacional de Investigaciones Cardiovasculares Carlos III (España) | |
dc.contributor.funder | Comunidad de Madrid (España) | |
dc.contributor.funder | Banco Santander | |
dc.contributor.funder | Fundación La Marató TV3 | |
dc.contributor.funder | Instituto de Salud Carlos III | |
dc.contributor.funder | Fundación ProCNIC | |
dc.contributor.funder | Ministerio de Ciencia e Innovación (España) | |
dc.description.peerreviewed | Sí | es_ES |
dc.relation.publisherversion | https://doi.org/10.3390/cancers13071525 | es_ES |
dc.identifier.journal | Cancers | 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/EC/H2020/ERC-2016-725091 | es_ES |
dc.rights.accessRights | open access | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/PID2019-108157RB | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/B2017/BMD-3733 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/201723 | es_ES |