Stuart G. Tangye, S. Cindy
Type I interferons (IFNs) are central to early antiviral innate immunity, being produced rapidly by diverse cell types to restrict viral replication.1 The importance of type I IFNs in host defence against infections became apparent in studies of mice treated with neutralising antibodies (Ab) against type I IFN, or rendered genetically deficient for the type I IFN receptors (IFNα/βR). Infection of these mice with a wide range of viruses resulted in severe morbidity and/or mortality.2 In contrast, control of bacterial or other non-viral pathogens in IFNα/βR-deficient mice was largely intact, while infection of mice lacking the type II IFNγR with these viruses was mild.