Publication
Mice lacking the known subunit of the type I interferon (IFN) receptor were completely unresponsive to type I IFNs, suggesting that this receptor chain is essential for type I IFN-mediated signal transduction. These mice showed no overt anomalies but were unable to cope with viral infections, despite otherwise normal immune responses. Comparison of mice lacking either type I or type II IFN receptors showed that, at least in response to some viruses, both IFN systems are essential for antiviral defense and are functionally nonredundant.
Jacques Fellay, Christian Axel Wandall Thorball, Shuting Xu
Jacques Fellay, Yu Zhang, Peng Zhang, Qian Zhang
Andrea Ablasser, Muhammet Fatih Gülen, Vivek Vijay Thacker, Théo Nass, Martin Schaller, Kunal Sharma