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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

An oxidative mechanism of interferon induced priming of the Fas pathway in Fanconi anemia cells.

Hematopoietic progenitor cells from children with Fanconi anemia of the C complementation group (FA-C) are excessively apoptotic and hypersensitive to various extracellular cues including Fas-ligand, tumor necrosis factor-alpha and double-stranded RNA. Interferon (IFN)-gamma is known to augment apoptotic responses of these factors. The "priming" effect of IFN-gamma is not fully explained. In view of the strong evidence that FA cells are intolerant of oxidative stress, we tested the notion that IFN-priming involves the induction of reactive oxygen species (ROS) in two FA-C B-lymphocyte cell lines and in peripheral blood neutrophils and mononuclear cells of FA patients. We also investigated whether the combination of IFN-gamma and Fas created an intracellular environment that promoted apoptosis. Significantly lower doses of IFN-gamma induced ROS accumulation in neutrophils and mononuclear cell of FA patients compared to cells of normal individuals. Enhanced ROS accumulation and decreased intracellular glutathione levels were observed in FA-C B-cell lines primed with IFN-gamma and treated with agonistic anti-Fas antibody than in isogenic control cells corrected with FANCC. The above treatment also induced caspase-3 and -8 activation as well as apoptosis. That antioxidants reduced the priming effect of IFN-gamma in Fas and IFN-gamma-treated FA lymphoblast cells, demonstrates that ROS represent a critical effector mechanism for the exaggerated responses to IFN-gamma characteristic of FA-C cells.[1]


  1. An oxidative mechanism of interferon induced priming of the Fas pathway in Fanconi anemia cells. Pearl-Yafe, M., Halperin, D., Halevy, A., Kalir, H., Bielorai, B., Fabian, I. Biochem. Pharmacol. (2003) [Pubmed]
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