[CD95 resistance and Fas ligand synthesis as mechanism of defense by immunocompetent cells in pancreatic tumors].
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.
D002470:Cell Survival / Q000276:immunology; D053222:Fas Ligand Protein; D006801:Humans; D008562:Membrane Glycoproteins / Q000378:metabolism*; D010190:Pancreatic Neoplasms / Q000276:immunology*; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology*; D014407:Tumor Cells, Cultured / Q000276:immunology*; D019139:Tumor Escape / Q000276:immunology*; D019014:fas Receptor / Q000276:immunology*
C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins; D019014:fas Receptor