dc.creator | Río, María Luisa del | es |
dc.creator | Yago-Díez de Juan, Carla | es |
dc.creator | Roncador, Giovanna | es |
dc.creator | Caleiras, Eduardo | es |
dc.creator | Álvarez-Esteban, Ramón | es |
dc.creator | Pérez Simón, José Antonio | es |
dc.creator | Rodríguez-Barbosa, José Ignacio | es |
dc.date.accessioned | 2024-04-30T13:47:20Z | |
dc.date.available | 2024-04-30T13:47:20Z | |
dc.date.issued | 2023 | |
dc.identifier.citation | Río, M.L.d., Yago-Díez de Juan, C., Roncador, G., Caleiras, E., Álvarez-Esteban, R., Pérez Simón, J.A. y Rodríguez-Barbosa, J.I. (2023). Genetic deletion of HVEM in a leukemia B cell line promotes a preferential increase of PD-1- stem cell-like T cells over PD-1+ T cells curbing tumor progression. Frontiers In Immunology, 14, 1113858. https://doi.org/10.3389/fimmu.2023.1113858. | |
dc.identifier.issn | 1664-3224 | es |
dc.identifier.uri | https://hdl.handle.net/11441/157359 | |
dc.description.abstract | Introduction: A high frequency of mutations affecting the gene encoding Herpes
Virus Entry Mediator (HVEM, TNFRSF14) is a common clinical finding in a wide
variety of human tumors, including those of hematological origin.
Methods: We have addressed how HVEM expression on A20 leukemia cells
influences tumor survival and its involvement in the modulation of the antitumor immune responses in a parental into F1 mouse tumor model of hybrid
resistance by knocking-out HVEM expression. HVEM WT or HVEM KO leukemia
cells were then injected intravenously into semiallogeneic F1 recipients and the
extent of tumor dissemination was evaluated.
Results: The loss of HVEM expression on A20 leukemia cells led to a significant
increase of lymphoid and myeloid tumor cell infiltration curbing tumor
progression. NK cells and to a lesser extent NKT cells and monocytes were the
predominant innate populations contributing to the global increase of immune
infiltrates in HVEM KO tumors compared to that present in HVEM KO tumors. In
the overall increase of the adaptive T cell immune infiltrates, the stem cell-like
PD-1- T cells progenitors and the effector T cell populations derived from them
were more prominently present than terminally differentiated PD-1+ T cells.
Conclusions: These results suggest that the PD-1- T cell subpopulation is likely
to be a more relevant contributor to tumor rejection than the PD-1+ T cell subpopulation. These findings highlight the role of co-inhibitory signals delivered
by HVEM upon engagement of BTLA on T cells and NK cells, placing HVEM/BTLA
interaction in the spotlight as a novel immune checkpoint for the reinforcement
of the anti-tumor responses in malignancies of hematopoietic origin. | es |
dc.format | application/pdf | es |
dc.format.extent | 19 p. | es |
dc.language.iso | eng | es |
dc.publisher | Frontiers Media S.A. | es |
dc.relation.ispartof | Frontiers In Immunology, 14, 1113858. | |
dc.rights | Atribución 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | * |
dc.subject | HVEM: herpesvirus entry mediator | es |
dc.subject | BTLA: B- and T-lymphocyte attenuator | es |
dc.subject | PD-1: programmed death 1 | es |
dc.subject | Tim 3: T-cell immunoglobulin and mucin-domain containing-3 | es |
dc.subject | Hybrid resistance | es |
dc.title | Genetic deletion of HVEM in a leukemia B cell line promotes a preferential increase of PD-1- stem cell-like T cells over PD-1+ T cells curbing tumor progression | es |
dc.type | info:eu-repo/semantics/article | es |
dc.type.version | info:eu-repo/semantics/publishedVersion | es |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | es |
dc.contributor.affiliation | Universidad de Sevilla. Departamento de Medicina | es |
dc.relation.projectID | PID2019-103984-RB-I00 | es |
dc.relation.projectID | PI16/00002 | es |
dc.relation.publisherversion | https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2023.1113858/full | es |
dc.identifier.doi | 10.3389/fimmu.2023.1113858 | es |
dc.journaltitle | Frontiers In Immunology | es |
dc.publication.volumen | 14 | es |
dc.publication.initialPage | 1113858 | es |
dc.contributor.funder | Ministerio de Ciencia y Universidades de España | es |
dc.contributor.funder | Instituto Carlos III | es |