Differential killing of pre-B acute lymphoblastic leukaemia cells by activated NK cells and the NK-92 ci cell line

Clin Exp Immunol. 2002 Aug;129(2):265-71. doi: 10.1046/j.1365-2249.2002.01919.x.

Abstract

The use of NK cells in adoptive therapy for malignant disease is an area of great potential. Currently the only NK cell line in clinical trials is NK-92, an activated NK cell line with a broad range of cytotoxicity against malignant cells. The activity of NK-92 against pre-B acute lymphoblastic leukaemias, however, is highly variable. In this study we compare the cytotoxic mechanisms and signalling pathways utilized by NK-92 ci and IL-2 activated NK cells to mediate killing of pre-B acute lymphoblastic leukaemia cell lines. Deficiencies in TNF family mediated apoptosis, phosphoinositide-3 kinase dependent and phosphoinositide-3 kinase independent killing limit the efficiency of NK-92 ci against pre-B acute lymphoblastic leukaemia cells. Importantly, treatment of the poorly killed leukaemia cells with TNF-alpha augmented both phosphoinositide-dependent and -independent cytolysis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis
  • Cell Line
  • Cytotoxicity, Immunologic
  • Humans
  • Immunotherapy, Adoptive
  • In Vitro Techniques
  • Interleukin-2 / pharmacology
  • Killer Cells, Natural / immunology*
  • Phosphatidylinositol 3-Kinases / metabolism
  • Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / enzymology
  • Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology*
  • Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / therapy*
  • Signal Transduction
  • Tumor Cells, Cultured
  • Tumor Necrosis Factor-alpha / metabolism
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Interleukin-2
  • Tumor Necrosis Factor-alpha
  • Phosphatidylinositol 3-Kinases