A FADD-dependent innate immune mechanism in mammalian cells

Siddharth Balachandran, Emmanuel Thomas and Glen N. Barber ()
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Siddharth Balachandran: University of Miami School of Medicine
Emmanuel Thomas: University of Miami School of Medicine
Glen N. Barber: University of Miami School of Medicine

Nature, 2004, vol. 432, issue 7015, 401-405

Abstract: Abstract Vertebrate innate immunity provides a first line of defence against pathogens such as viruses and bacteria. Viral infection activates a potent innate immune response, which can be triggered by double-stranded (ds)RNA produced during viral replication1,2,3. Here, we report that mammalian cells lacking the death-domain-containing protein FADD4,5 are defective in intracellular dsRNA-activated gene expression, including production of type I (α/β) interferons, and are thus very susceptible to viral infection. The signalling pathway incorporating FADD is largely independent of Toll-like receptor 3 and the dsRNA-dependent kinase PKR, but seems to require receptor interacting protein 1 as well as Tank-binding kinase 1-mediated activation of the transcription factor IRF-3. The requirement for FADD in mammalian host defence is evocative of innate immune signalling in Drosophila, in which a FADD-dependent pathway responds to bacterial infection by activating the transcription of antimicrobial genes6. These data therefore suggest the existence of a conserved pathogen recognition pathway in mammalian cells that is essential for the optimal induction of type I interferons and other genes important for host defence.

Date: 2004
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DOI: 10.1038/nature03124

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