CD95 resistance and Fas ligand synthesis as mechanism of defense by immunocompetent cells in pancreatic tumors
Ungefroren, H.; Voss, M.; Henne-Bruns, D.; Kremer, B.; Kalthoff, H.
Langenbecks Archiv für Chirurgie. Suppl. Kongressband. Deutsche Gesellschaft für Chirurgie. Kongress 115(Suppl I): 63-67
1998
ISSN/ISBN: 0942-2854 PMID: 14518214 Document Number: 485736
Tumor cells have developed a variety of passive and active strategies to escape surveillance by the host immune system. In the present work we have investigated the role of the CD95 system comprising the CD95 receptor (Fas, CD95, APO-1) and its ligand Fas-ligand (FasL) in the dialogue between pancreatic tumor cells and tumor-reactive/cytotoxic T cells. Despite abundant expression of CD95 in pancreatic tumor cells from tumor tissue and in various pancreatic tumor cell lines, we found all (6/6) pancreatic tumor cell lines to be largely resistant to CD95-mediated apoptosis when compared to the CD95-sensitive T cell line Jurkat. Intriguingly, all pancreatic tumor cell lines tested synthesized FasL. In coculture experiments it was shown that two were capable of increasing Jurkat cell apoptosis in a FasL-dependent manner. These data suggest that pancreatic tumor cells have exploited the CD95 system to their benefit in order to protect themselves against tumor-reactive T cells.