dc.creator | Ascui, Gabriel | |
dc.creator | Gálvez Jirón, Felipe | |
dc.creator | Kramm, Karina | |
dc.creator | Schafer, Carolina | |
dc.creator | Siña, Josefina | |
dc.creator | Pola, Víctor | |
dc.creator | Cristi, Francisca | |
dc.creator | Hernández, Carolina | |
dc.creator | Garrido Tapia, Macarena | |
dc.creator | Pesce Reyes, Bárbara | |
dc.creator | Bustamante Zamorano, Marco | |
dc.creator | Fluxá Rojas, Paula | |
dc.creator | Molina Sampayo, María Carmen | |
dc.creator | Ribeiro, Carolina H. | |
dc.date.accessioned | 2020-06-03T15:15:35Z | |
dc.date.available | 2020-06-03T15:15:35Z | |
dc.date.created | 2020-06-03T15:15:35Z | |
dc.date.issued | 2020 | |
dc.identifier | Immunology & Cell Biology 2020; 1–14 | |
dc.identifier | 10.1111/imcb.12331 | |
dc.identifier | https://repositorio.uchile.cl/handle/2250/175184 | |
dc.description.abstract | Gastric 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. | |
dc.language | en | |
dc.publisher | Wiley | |
dc.rights | http://creativecommons.org/licenses/by-nc-nd/3.0/cl/ | |
dc.rights | Attribution-NonCommercial-NoDerivs 3.0 Chile | |
dc.source | Immunology & Cell Biology | |
dc.subject | CD1d | |
dc.subject | Cytotoxicity | |
dc.subject | Gastric cancer | |
dc.subject | INKT cells | |
dc.subject | NKG2D receptor | |
dc.title | Decreased invariant natural killer T-cell-mediated antitumor immune response in patients with gastric cancer | |
dc.type | Artículo de revista | |