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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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Evolutionary Origins of cGAS-STING Signaling

TL;DR: The evolutionary origins of the cGAS-STING pathway are discussed, and the possibility that the ancestral functions of STING may have included activation of antibacterial immunity is considered.
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The interferon in TLR signaling: more than just antiviral

TL;DR: The Toll-like receptor system is responsible for the recognition of infectious agents leading to initiation of the primary innate, and later adaptive, immune response and type I interferons, which were discovered as antiviral proteins, are now known to be produced in response to TLR activation by many pathogens, including bacteria.
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Type I IFN Receptor Signals Directly Stimulate Local B Cells Early following Influenza Virus Infection

TL;DR: It is shown that the first direct stimulatory signal for local respiratory tract B cells during influenza virus infection is provided through the type I IFNR, and ligand(s) of this IFNR are direct nonredundant early innate signals that regulate local antiviral B cell responses.
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Vaccinia virus blocks gamma interferon signal transduction: viral VH1 phosphatase reverses Stat1 activation.

TL;DR: A novel mechanism by which vaccinia virus interferes with the onset of host immune responses by blocking the IFN-γ signal cascade through the dephosphorylating activity of the viral phosphatase VH1 is revealed.
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Macrophage-expressed IFN-β Contributes to Apoptotic Alveolar Epithelial Cell Injury in Severe Influenza Virus Pneumonia

TL;DR: It is demonstrated that macrophage-released type I IFNs contribute to IV-induced AEC damage and lung injury by autocrine induction of the pro-apoptotic factor TRAIL and suggested that therapeutic targeting of the macrophages IFN-β-TRAIL axis might represent a promising strategy to attenuate IV- induced acute lung injury.
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.
Journal ArticleDOI

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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