Metabolic inhibitors render "resistant" target cells sensitive to natural killer cell-mediated lysis.
L-929 cells were lysed by activated but not by endogenous natural killer (NK) cells, as reported previously. Nevertheless, L-929 cells bound to endogenous NK cells, as shown by target binding cell, cold target competition, and monolayer absorption assays. Treatment of L-929 cells with actinomycin-D or cycloheximide rendered them sensitive to lysis by endogenous NK cells and markedly increased their sensitivity to lysis by activated NK cells. Treatment with these drugs under the prescribed conditions did not affect the binding of L-929 cells to NK cells. Since others have shown that treatment with these drugs inhibits membrane repair processes and renders cells more sensitive to complement-mediated lysis, we hypothesize that membrane repair may be an important factor influencing a cell sensitivity to NK cells. This may be more important than NK-binding ability, since most cells can be lysed by (and therefore bind to) activated NK cells.
D000818:Animals; D002460:Cell Line; D003513:Cycloheximide / Q000494:pharmacology*; D003601:Cytotoxicity Tests, Immunologic; D003609:Dactinomycin / Q000494:pharmacology*; D007694:Killer Cells, Natural / Q000276:immunology*; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA
D003609:Dactinomycin; D003513:Cycloheximide