Impact of FASL-induced apoptosis in the elimination of tumor cells by NK cells

Mol Immunol. 2005 Feb;42(4):495-9. doi: 10.1016/j.molimm.2004.07.033.


The cytotoxic effector functions of NK cells are important for enabling the immune system to cope efficiently with infection and malignancy. Two major mechanisms of cytotoxicity are perforin/granzyme- and death receptor-mediated (e.g., FASL- or TRAIL-mediated) induction of cell death. Many studies, including studies in perforin-deficient animals, have led to the conclusion that perforin/granzyme-mediated induction of cell death is a principal pathway used by NK cells to eliminate virus-infected or transformed cells. However, death receptor-mediated apoptosis may also contribute to NK cell-mediated cytotoxicity, as revealed by more recent reports. In the present paper, we have reviewed current data on death receptor-mediated tumor cell apoptosis by NK cells with a particular emphasis on the role of NK cell FASL in the RMA/RMA-S tumor model.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis / immunology
  • Apoptosis / physiology*
  • Cytotoxicity, Immunologic*
  • Fas Ligand Protein
  • Humans
  • Killer Cells, Natural / immunology*
  • Membrane Glycoproteins / immunology
  • Membrane Glycoproteins / physiology*
  • Mice
  • Neoplasms / immunology*
  • Perforin
  • Pore Forming Cytotoxic Proteins
  • Serine Endopeptidases / physiology


  • FASLG protein, human
  • Fas Ligand Protein
  • Fasl protein, mouse
  • Membrane Glycoproteins
  • Pore Forming Cytotoxic Proteins
  • Perforin
  • Serine Endopeptidases