Increased sensitivity to natural killing in Raji cells is due to effector recognition of molecules appearing on target cell membranes following EBV cycle induction.
Previous studies demonstrated that NK resistant Epstein-Barr virus (EBV) carrying human lymphoblastoid cell lines become sensitive to NK cell-mediated destruction following induction of the viral cycle by superinfection with the P3HR-1 substrain of EBV or chemicals. In the present report we analysed the cellular membrane changes that were related to the development of sensitivity to NK activity in Raji cells with metabolic inhibitors. NK sensitivity does not develop in P3HR-1 superinfected Raji cells that are cultured in the presence of the RNA synthesis inhibitor actinomycin D and drops to half the amount usually detected in superinfected cells that are grown with the protein synthesis inhibitor cyclohexamide. In experiments with cyclohexamide blocks removed after 24 h, the target cell sensitivity to NK returns to normal levels. Control Raji cells cultured with the same inhibitors for up to 72 h do not develop any sensitivity to NK cell activity. These findings suggest that the development of sensitivity to NK destruction in Raji cells following superinfection is due to the addition to the cell membrane of a virally promoted molecule(s) that requires active RNA and protein synthesis.
D002051:Burkitt Lymphoma / Q000276:immunology; D002460:Cell Line; D002462:Cell Membrane / Q000276:immunology*; D002478:Cells, Cultured; D003513:Cycloheximide / Q000494:pharmacology; D003609:Dactinomycin / Q000494:pharmacology; D004854:Herpesvirus 4, Human / Q000276:immunology*; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology*; D009363:Neoplasm Proteins / Q000096:biosynthesis; D012334:RNA, Neoplasm / Q000096:biosynthesis
D009363:Neoplasm Proteins; D012334:RNA, Neoplasm; D003609:Dactinomycin; D003513:Cycloheximide