Publication Date:
1994-06-24
Description:
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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller, U -- Steinhoff, U -- Reis, L F -- Hemmi, S -- Pavlovic, J -- Zinkernagel, R M -- Aguet, M -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1918-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Biology I, University of Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8009221" target="_blank"〉PubMed〈/a〉
Keywords:
Alphavirus Infections/immunology
;
Animals
;
Antibodies, Viral/biosynthesis
;
Disease Susceptibility
;
Immunity, Innate
;
Interferon Type I/*physiology
;
Interferon-gamma/*physiology
;
Lymphocytic Choriomeningitis/immunology
;
Membrane Proteins
;
Mice
;
Mutation
;
Receptor, Interferon alpha-beta
;
Receptors, Interferon/genetics/*physiology
;
Rhabdoviridae Infections/immunology
;
Semliki forest virus
;
Signal Transduction
;
T-Lymphocytes/immunology
;
Vesicular stomatitis Indiana virus
;
Virus Diseases/*immunology
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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