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Nature 434, 772-777 (30 March 2005) | doi:10.1038/nature03464;
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Director, Division of Materials Research
- National Science Foundation
- Arlington, VA
Postdoctoral Research in Functional Genomics
- Harvard School of Public Health, computer science, biology, bioinformatics,
- Boston, MA
IRF-7 is the master regulator of type-I interferon-dependent immune responses
The type-I interferon (IFN-α/β) response is critical to immunity against viruses and can be triggered in many cell types by cytosolic detection of viral infection, or in differentiated plasmacytoid dendritic cells by the Toll-like receptor 9 (TLR9) subfamily, which generates signals via the adaptor MyD88 to elicit robust IFN induction. Using mice deficient in the Irf7 gene (Irf7-/- mice), we show that the transcription factor IRF-7 is essential for the induction of IFN-α/β genes via the virus-activated, MyD88-independent pathway and the TLR-activated, MyD88-dependent pathway.
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