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Letters to Nature
Nature 432, 401-405 (18 November 2004) | doi:10.1038/nature03124; Received 1 August 2004; Accepted 15 October 2004
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Postdoctoral Fellowship
- Lovelace Respiratory Research Institute
- Albuquerque, New Mexico
Behavioural Pharmacologist
- Eisai London Research Laboratories Ltd
- Hatfield, United Kingdom
A FADD-dependent innate immune mechanism in mammalian cells
Siddharth Balachandran1,2, Emmanuel Thomas1,2 & Glen N. Barber
- Department of Microbiology and Immunology and Sylvester Comprehensive Cancer Center, University of Miami School of Medicine, Miami, Florida 33136, USA
- These authors contributed equally to this work
Correspondence to: Glen N. Barber Email: gbarber@med.miami.edu
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 (
/
) 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.
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