Induction of Fas Ligand-Mediated Apoptosis by Interferon-α

Interferon-α (IFN-α) 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-α to augment NK cell cytotoxicity against virus-infected target cells or tumor cells is well established, t...

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Bibliographic Details
Published in:Clinical immunology (Orlando, Fla.) Fla.), 2000-06, Vol.95 (3), p.218-226
Main Authors: Kirou, Kyriakos A., Krishna, Radha, Maria, Vakkalanka, Butler, J., Crow, Mary K.
Format: Article
Language:English
Subjects:
apoptosis
Apoptosis - drug effects
Biological and medical sciences
cytokines
Cytotoxicity, Immunologic - drug effects
Dose-Response Relationship, Immunologic
FACS
Fas Ligand Protein
Fundamental and applied biological sciences. Psychology
Fundamental immunology
human
Humans
Immunobiology
Interferon-alpha - pharmacology
Killer Cells, Natural - chemistry
Leukocytes, Mononuclear - chemistry
Ligands
Membrane Glycoproteins - drug effects
Membrane Glycoproteins - genetics
Membrane Glycoproteins - pharmacology
Modulation of the immune response (stimulation, suppression)
NK cells
RNA, Messenger - blood
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Summary:Interferon-α (IFN-α) 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-α 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-α 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-α 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-α 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.
ISSN:1521-6616
1521-7035
DOI:10.1006/clim.2000.4866