Abstract
We have investigated the effect of interferon‐gamma (IFN‐γ) treatment of neuroblastoma cells on the susceptibility to lysis by lymphokine‐activated killer (LAK) cells and examined the participation of cell‐adhesion molecules on the target cells in LAK cell lysis. Untreated neuroblastoma cells expressed lymphocyte‐function‐associated antigen 3 (LFA‐3) and neural‐cell‐adhesion molecule (NCAM), but did not express MHC‐class‐I, MHC‐class‐II, or intercellular‐adhesion molecule 1 (ICAM‐1). IFN‐γ treatment of neuroblastoma cells induced the expression of MHC‐class‐I and ICAM‐1 antigens, but did not affect the expression of MHC‐class‐II, LFA‐3, and NCAM. This was accompanied by an increased susceptibility to lysis by LAK cells. Anti‐ICAM‐1 antibody inhibited partially the increased sensitivity of IFN‐γ‐treated neuroblastoma cells to LAK cell lysis, and blocked completely the increase in binding of LAK cells observed after IFN‐γ treatment of the target cells. These results suggest that the increased LAK sensitivity of IFN‐γ‐treated neuroblastoma cells is partially attributable to the induction of ICAM‐1 on neuroblastoma cells and indicate that post‐binding events also play a role in the increased sensitivity to LAK cell lysis observed after IFN‐γ treatment.