Target Cell Membrane Modification and Susceptibility to Lymphokine-Activated Killer Cell-Mediated Lysis: II. Sodium Periodate Has a Differential Effect on the Lysis of Human and Murine Tumor Cells

Abstract

Little is known about the mechanism by which lymphokine-activated killer (LAK) cells and natural killer (NK) cells recognize and lyse target cells. We undertook this study to investigate the effects of target cell membrane modification by sodium periodate (PI) on the lysis of tumor cells by human and murine LAK cells (HLAK, MLAK) and NK cells (HNK, MNK). LAK and NK cells were generated and used as effector cells in 4-hr 51 Cr release assays against a variety of PI-treated and untreated target cells. PI significantly increased the MLAK cell-mediated lysis of YAC and MH134 tumor cells, but had no effect on the MNK lysis of YAC or MH134 tumor cells. PI had no effect on the HLAK or HNK lysis of YAC or MH134 tumor cells. PI had no effect on the MLAK or MNK lysis of K562 or U937 human tumor cells. Similarly, PI had no effect on the HLAK lysis of K562, but did significantly increase the HNK lysis of K562. PI increased both the HLAK and HNK lysis of U937. Cold target inhibition studies revealed that PI-treated YAC cells inhibited the MLAK cell-mediated lysis of untreated YAC cells. The variable effects of PI on LAK cell- and NK cell-mediated lysis support the hypothesis that LAK cells are a distinct population of cells rather than a subpopulation of NK cells on the basis of mechanism of target cell recognition. The results of the cold target inhibition study suggest that PI-treated tumor cells are identified by effector cells in a manner similar to that of untreated cells. Human and murine effector cells also demonstrate species differences that may be important for the design of future studies.