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Journal ArticleDOI

Functional role of type I and type II interferons in antiviral defense.

TLDR
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.
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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Journal ArticleDOI

Respiratory epithelial cells in innate immunity to influenza virus infection

TL;DR: This review details immune events during influenza infection from the viewpoint of the epithelial cells, secretory host defense mechanisms, cell death, and recovery.
Journal ArticleDOI

Mechanism of Virulence Attenuation of Glycosaminoglycan-Binding Variants of Japanese Encephalitis Virus and Murray Valley Encephalitis Virus

TL;DR: It is found that GAG-binding variants of JEV and MVE were rapidly removed from the bloodstream and failed to spread from extraneural sites of replication into the brain, suggesting that the enhanced affinity of the attenuated variants for GAGs ubiquitously present on cells and extracellular matrices most likely prevented viremia of sufficient magnitude and/or duration required for virus entry into thebrain parenchyma.
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Type I IFN signaling triggers immunopathology in tuberculosis‐susceptible mice by modulating lung phagocyte dynamics

TL;DR: It is concluded that IFN I alters early innate events at the site of Mtb invasion leading to fatal immunopathology, furnish a mechanistic explanation for the detrimental role of IFn I in pulmonary TB and form a basis for understanding the complex roles ofIFN I in chronic inflammation.
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Interferon-Induced Ifit2/ISG54 Protects Mice from Lethal VSV Neuropathogenesis

TL;DR: In Ifit2 knockout (Ifit2 −/−) mice, intranasal VSV infection was uniformly lethal and death was preceded by neurological signs, such as ataxia and hind limb paralysis, and this study provides a clear demonstration of tissue-, virus- and ISG-specific antiviral action of interferon.
Journal ArticleDOI

Viral infections in interferon-γ receptor deficiency

TL;DR: It is concluded that patients with interferon-γ receptor deficiency and mycobacterial disease have increased susceptibility to some viral pathogens.
References
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Journal ArticleDOI

Various rat adult tissues express only one major mRNA species from the glyceraldehyde-3-phosphate-dehydrogenase multigenic family

TL;DR: This sequence allowed the determination of the hitherto unknown primary structure of rat GAPDH which is 333 aminoacids long and revealed a high degree of sequence conservation at both nucleotide and protein levels.
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Disruption of the proto-oncogene int-2 in mouse embryo-derived stem cells: a general strategy for targeting mutations to non-selectable genes

TL;DR: A positive and negative selection procedure is described that enriches 2,000-fold for those cells that contain a targeted mutation in mouse embryo-derived stem cells.
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Immune response in mice that lack the interferon-gamma receptor.

TL;DR: Mutant mice offer the possibility for the further elucidation of IFN-gamma-mediated functions by transgenic cell- or tissue-specific reconstitution of a functional receptor.
Journal ArticleDOI

Regulated expression of a gene encoding a nuclear factor, IRF-1, that specifically binds to IFN-β gene regulatory elements

TL;DR: It is shown here that the IRF-1 gene possesses virus-inducible promoter and is also involved in the regulation of other genes such as IFN-alpha and MHC class I genes.
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