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Nasopharyngeal carcinomas (NPC) are human epithelial tumors constantly associated with the Epstein-Barr virus. However it was known that these cells were producing in vitro exosomes carrying the galectin 9 protein. Galectin 9 is an agonist of the Tim-3 receptor, a pro-apoptotic receptor carried by the mature CD4 + Th1 lymphocytes. Our data show that NPC exosomes carrying galectin 9 behave as agonists of the Tim-3 receptor. They are selectively detected in the plasma of xenografted mice or patients with NPC. In vitro they induce massive apoptosis of cells derived from CD4 + Th1 lymphocyte…mehr

Produktbeschreibung
Nasopharyngeal carcinomas (NPC) are human epithelial tumors constantly associated with the Epstein-Barr virus. However it was known that these cells were producing in vitro exosomes carrying the galectin 9 protein. Galectin 9 is an agonist of the Tim-3 receptor, a pro-apoptotic receptor carried by the mature CD4 + Th1 lymphocytes. Our data show that NPC exosomes carrying galectin 9 behave as agonists of the Tim-3 receptor. They are selectively detected in the plasma of xenografted mice or patients with NPC. In vitro they induce massive apoptosis of cells derived from CD4 + Th1 lymphocyte clones expressing Tim-3 and used as a model of cellular targets. This effect is inhibited by pre-incubating either the target cells with an anti-Tim-3 blocking antibody or the exosomes with an anti-galectin 9 antibody. Overall, our work suggests that NPC exosomes carrying galectin 9 play an important role as a factor of immunosuppression in NPC patients. Patient treatment with anti-galectin 9 antibodies might be beneficial in combination with some protocols of adoptive immunotherapy.
Autorenporträt
Les cellules de carcinomes nasopharyngés (NPC) produisent des exosomes véhiculant la galectine 9. Ces exosomes jouent un rôle important comme facteur d''immunosuppression chez les malades porteurs de NPC. ces exosomes aident à l''identification de nouveaux biomarqueurs utiles au dépistage précoce ou à la surveillance thérapeutique.