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Increased susceptibility of ifn‐γ‐treated neuroblastoma cells to lysis by lymphokine‐activated killer cells: Participation of ICAM‐1 induction on target cells
Author(s) -
Naganuma Hirofumi,
Kiessling Rolf,
Patarroyo Manuel,
Hansson Mona,
Handgretinger Rupert,
Grönberg Alvar
Publication year - 1991
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910470410
Subject(s) - lymphokine activated killer cell , lymphokine , neuroblastoma , neural cell adhesion molecule , biology , major histocompatibility complex , lymphocyte function associated antigen 1 , cell adhesion molecule , cytotoxic t cell , cytolysis , lymphocyte , antigen , microbiology and biotechnology , immunology , cell adhesion , cancer research , cell , interleukin 21 , cell culture , intercellular adhesion molecule 1 , cd8 , in vitro , biochemistry , genetics
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.