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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Alphavirus Infections / immunology
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Animals
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Antibodies, Viral / biosynthesis
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Disease Susceptibility
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Immunity, Innate
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Interferon Type I / physiology*
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Interferon gamma Receptor
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Interferon-gamma / physiology*
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Lymphocytic Choriomeningitis / immunology
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Membrane Proteins
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Mice
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Mutation
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Receptor, Interferon alpha-beta
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Receptors, Interferon / genetics
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Receptors, Interferon / physiology*
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Rhabdoviridae Infections / immunology
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Semliki forest virus
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Signal Transduction
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T-Lymphocytes / immunology
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Vesicular stomatitis Indiana virus
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Virus Diseases / immunology*
Substances
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Antibodies, Viral
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Interferon Type I
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Membrane Proteins
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Receptors, Interferon
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Receptor, Interferon alpha-beta
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Interferon-gamma