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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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Cytokines in Sepsis: Potent Immunoregulators and Potential Therapeutic Targets—An Updated View

TL;DR: This review addresses the current knowledge of the actions of pro- and anti-inflammatory cytokines in sepsis pathophysiology as well as how these cytokines and other important immunomodulating agents may be therapeutically targeted to improve the clinical outcome of sepsi.
Journal ArticleDOI

Interferon signalling network in innate defence.

TL;DR: Further comprehensive understanding of IFN signalling may offer a better direction to unravelling the complex signalling networks in the host defence system, and may contribute to their more effective therapeutic applications.
Journal ArticleDOI

Apoptotic Caspases Prevent the Induction of Type I Interferons by Mitochondrial DNA

TL;DR: The results show that mitochondria have the capacity to simultaneously expose a cell-intrinsic inducer of the IFN response and to inactivate this response in a caspase-dependent manner, which provides a dual control, which determines whether mitochondria initiate an immunologically silent or a proinflammatory type of cell death.
Journal ArticleDOI

A mouse model for Chikungunya: young age and inefficient type-I interferon signaling are risk factors for severe disease.

TL;DR: It is shown that whereas wild type (WT) adult mice are resistant to CHIKV infection, WT mouse neonates are susceptible and neonatal disease severity is age-dependent, and the neonatal phase and inefficient type-I IFN signaling as risk factors for severe CHikV-associated disease are identified.
Journal ArticleDOI

Type-I interferon receptor deficiency reduces lupus-like disease in NZB mice.

TL;DR: The data indicate that type-I IFNs are important mediators in the pathogenesis of murine lupus, and that reducing their activity in the human counterpart may be beneficial.
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.
Journal ArticleDOI

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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