[Significance if ICAM-1 on lysis of human pancreatic carcinoma cells by autologous, cytotoxic T-lymphocytes].
Cytotoxic T-Lymphocytes were generated from tumor-infiltrating lymphocytes of a newly established pancreatic cancer cell line, which lysed autologous tumor cells significantly and HLA-class I restricted. ICAM-1+ tumor clones were significantly higher lysed than an ICAM-1- clone. Stimulation with IFN-gamma resulted in a higher expression of ICAM-1 and significantly higher lysis, which was inhibited by anti-ICAM-1 monoclonal antibodies.
D000230:Adenocarcinoma / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D003001:Cloning, Molecular; D003602:Cytotoxicity, Immunologic / Q000235:genetics / Q000276:immunology*; D015972:Gene Expression Regulation, Neoplastic / Q000502:physiology; D015395:Histocompatibility Antigens Class I / Q000235:genetics / Q000276:immunology; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics*; D016246:Lymphocytes, Tumor-Infiltrating / Q000276:immunology*; D010190:Pancreatic Neoplasms / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology*; D014407:Tumor Cells, Cultured / Q000276:immunology* / Q000473:pathology
D015395:Histocompatibility Antigens Class I; D018799:Intercellular Adhesion Molecule-1