Active tumor cell resistance to human natural killer lymphocyte attack.
Inhibition of protein synthesis by cycloheximide, puromycin, or emetine increased tumor lysis mediated by human natural killer (NK) cells to "slow" but not "fast" tumor targets. Human T24 bladder carcinoma cells were used as slow targets which are killed after a approximately 3-hr lag period, and K562 cells derived from a patient with myelogenous leukemia were used as fast targets which are killed without a lag period. This enhancement of killing exceeded that which would have been expected simply from a reduction of tumor cell growth during the time of assay. Pretreatment of the NK effector cells and the tumor cells separately showed that the effect was on the tumor cells and not due to enhancement of NK cell activity. These observations imply that some tumor cells can actively resist NK attack. The discovery that some but not all human tumor cells actively resist cellular immune attack, perhaps by repair mechanisms dependent upon protein synthesis, provides a new model for evaluation of tumor cells in their resistance to host defenses.
D002460:Cell Line; D003513:Cycloheximide / Q000494:pharmacology; D004640:Emetine / Q000494:pharmacology; D006801:Humans; D007694:Killer Cells, Natural / Q000187:drug effects / Q000276:immunology*; D007938:Leukemia; D009369:Neoplasms / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D014176:Protein Biosynthesis; D011691:Puromycin / Q000494:pharmacology; D013997:Time Factors; D001749:Urinary Bladder Neoplasms
D011691:Puromycin; D003513:Cycloheximide; D004640:Emetine