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Abstract

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.

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Science
Volume 264 | Issue 5167
24 June 1994

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Published in print: 24 June 1994

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Ulrike Müller
Institute of Molecular Biology I, University of Zürich, Hönggerberg, 8093 Zürich, Switzerland.
Ulrich Steinhoff
Institute of Molecular Biology I, University of Zürich, Hönggerberg, 8093 Zürich, Switzerland.
Luiz F. L. Reis
Institute of Molecular Biology I, University of Zürich, Hönggerberg, 8093 Zürich, Switzerland.
Silvio Hemmi
Institute of Molecular Biology I, University of Zürich, Hönggerberg, 8093 Zürich, Switzerland.
Jovan Pavlovic
Institute of Medical Virology, University of Zürich, 8028 Zürich, Switzerland.
Rolf M. Zinkernagel
Institute of Molecular Biology I, University of Zürich, Hönggerberg, 8093 Zürich, Switzerland.
Michel Aguet
Institute of Molecular Biology I, University of Zürich, Hönggerberg, 8093 Zürich, Switzerland.

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