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Authordc.contributor.authorAscui, Gabriel 
Authordc.contributor.authorGálvez Jirón, Felipe 
Authordc.contributor.authorKramm, Karina 
Authordc.contributor.authorSchafer, Carolina 
Authordc.contributor.authorSiña, Josefina 
Authordc.contributor.authorPola, Víctor 
Authordc.contributor.authorCristi, Francisca 
Authordc.contributor.authorHernández, Carolina 
Authordc.contributor.authorGarrido Tapia, Macarena 
Authordc.contributor.authorPesce Reyes, Bárbara 
Authordc.contributor.authorBustamante Zamorano, Marco 
Authordc.contributor.authorFluxá Rojas, Paula 
Authordc.contributor.authorMolina Sampayo, María Carmen 
Authordc.contributor.authorRibeiro, Carolina H. 
Admission datedc.date.accessioned2020-06-03T15:15:35Z
Available datedc.date.available2020-06-03T15:15:35Z
Publication datedc.date.issued2020
Cita de ítemdc.identifier.citationImmunology & Cell Biology 2020; 1–14es_ES
Identifierdc.identifier.other10.1111/imcb.12331
Identifierdc.identifier.urihttps://repositorio.uchile.cl/handle/2250/175184
Abstractdc.description.abstractGastric cancer (GC) is the third most common cause of cancer-related death worldwide. Invariant natural killer T (iNKT) cells are innate-like cytotoxic T lymphocytes involved in tumor immune surveillance. They can be activated either through CD1d-presented glycolipid antigens recognized by their invariant T-cell receptor, cytokines or by sensing tumor-associated stress-induced ligands through the natural killer group 2, member D (NKG2D) receptor. Although the number and functionality of iNKT cells may be decreased in several types of cancer, here we show that GC patients presented a mild increase in iNKT cell frequencies and numbers in the blood compared with healthy donors. In GC patients, iNKT cells, expanded in vitro with alpha-galactosyl ceramide and stimulated with phorbol 12-myristate 13-acetate and ionomycin, produced higher levels of interleukin-2 and transforming growth factor-beta, while their capacity to degranulate remained preserved. Because tumor-derived epithelial cell adhesion molecule-positive epithelial cells did not display surface CD1d, and NKG2D ligands (NKG2DLs) were detected in the gastric tumor milieu, we envisioned a role for NKG2D in iNKT cell functions. Peripheral iNKT cells from GC patients and controls presented similar levels of NKG2D; nevertheless, the percentages of interferon-gamma-producing and CD107a-positive iNKT cells from patients were reduced upon challenge with CD1d-negative, NKG2DL-positive K562 cells, suggesting a compromised response by iNKT cells in GC patients, which may not result from impaired NKG2D/NKG2DL signaling. The decreased response of iNKT cells may explain the fact that higher frequencies of circulating iNKT cells did not confer a survival benefit for GC patients. Therefore, functional impairment of iNKT cells in GC may contribute to tumor immune escape and favor disease progression.es_ES
Patrocinadordc.description.sponsorshipComision Nacional de Investigacion Cientifica y Tecnologica (CONICYT) CONICYT FONDECYT 11110456 1130330 University of Chile ENLACE-VID ENL012/15 Biomedical Sciences Institute (ICBM) Funding Grant 2018 Comision Nacional de Investigacion Cientifica y Tecnologica (CONICYT) FONDEQUIP140032 AIC-08 ICBM, School of Medicine of University of Chile, Santiago, Chilees_ES
Lenguagedc.language.isoenes_ES
Publisherdc.publisherWileyes_ES
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile*
Link to Licensedc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/*
Sourcedc.sourceImmunology & Cell Biologyes_ES
Keywordsdc.subjectCD1des_ES
Keywordsdc.subjectCytotoxicityes_ES
Keywordsdc.subjectGastric canceres_ES
Keywordsdc.subjectINKT cellses_ES
Keywordsdc.subjectNKG2D receptores_ES
Títulodc.titleDecreased invariant natural killer T-cell-mediated antitumor immune response in patients with gastric canceres_ES
Document typedc.typeArtículo de revistaes_ES
dcterms.accessRightsdcterms.accessRightsAcceso Abierto
Catalogueruchile.catalogadorcrbes_ES
Indexationuchile.indexArtículo de publicación ISI
Indexationuchile.indexArtículo de publicación SCOPUS


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Attribution-NonCommercial-NoDerivs 3.0 Chile
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile