Induction of Fas ligand-mediated apoptosis by interferon-alpha. Academic Article uri icon

Overview

MeSH

  • Cytotoxicity, Immunologic
  • Dose-Response Relationship, Immunologic
  • Fas Ligand Protein
  • Humans
  • Killer Cells, Natural
  • Leukocytes, Mononuclear
  • Ligands
  • RNA, Messenger

MeSH Major

  • Apoptosis
  • Interferon-alpha
  • Membrane Glycoproteins

abstract

  • Interferon-alpha (IFN-alpha) was among the first cytokines studied and the earliest to be used in clinical medicine for the treatment of viral infections and malignancies. Although the capacity of IFN-alpha to augment NK cell cytotoxicity against virus-infected target cells or tumor cells is well established, the mechanism has not been fully elucidated. Here we report that IFN-alpha stimulation of PBMC from healthy donors induces Fas (CD95) ligand (FasL) transcription and leads to increased cell surface FasL expression exclusively on the NK cell fraction. Furthermore, IFN-alpha augments the FasL-mediated cytotoxicity of normal PBMC against Fas-sensitive lymphoid tumor cells. In the context of innate immunity, induction of FasL by IFN-alpha can be viewed as an efficient mechanism to potentiate NK cell cytotoxicity in the presence of harmful targets, such as virally infected or transformed cells.

publication date

  • June 2000

has subject area

  • Apoptosis
  • Cytotoxicity, Immunologic
  • Dose-Response Relationship, Immunologic
  • Fas Ligand Protein
  • Humans
  • Interferon-alpha
  • Killer Cells, Natural
  • Leukocytes, Mononuclear
  • Ligands
  • Membrane Glycoproteins
  • RNA, Messenger

Research

keywords

  • Journal Article

Identity

Language

  • eng

PubMed ID

  • 10866129

Additional Document Info

start page

  • 218

end page

  • 226

volume

  • 95

number

  • 3