Mice lacking the known subunit of the type I interferon (IFN) receptor
were completely unresponsive to type I IFNs, suggesting that this rec
eptor chain is essential for type I IFN-mediated signal transduction.
These mice showed no overt anomalies but were unable to cope with vira
l infections, despite otherwise normal immune responses. Comparison of
mice lacking either type I or type II IFN receptors showed that, at l
east in response to some viruses, both IFN systems are essential for a
ntiviral defense and are functionally nonredundant.