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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

T Cell-Derived IL-10 Impairs Host Resistance to Mycobacterium tuberculosis Infection.

TL;DR: Data reveal that, despite the multiple immune sources of IL-10 during M. tuberculosis infection, activated effector T cells are the major source accounting for IL- 10–induced TB susceptibility.
Journal Article

Compromised virus control and augmented perforin-mediated immunopathology in IFN-gamma-deficient mice infected with lymphocytic choriomeningitis virus.

TL;DR: The results reveal that IFN-gamma is pivotal to T cell-mediated control of a rapidly invasive stain, whereas it is less important in the acute elimination of a slowly invasive strain.
Journal ArticleDOI

Type I interferons and limitin: a comparison of structures, receptors, and functions

TL;DR: Lim limitin this paper is a type I interferon (IFN)-like molecule that has weak sequence homology to IFN-alpha,IFN-beta, and IFNomega and displays its biological functions through the same IFNα/β receptors.
Journal ArticleDOI

ISG15 Arg151 and the ISG15-conjugating enzyme UbE1L are important for innate immune control of Sindbis virus.

TL;DR: A role for protein conjugation in the antiviral effects of ISG15 is assessed by constructing double subgenomic Sindbis viruses that expressed the mISG15 R151A mutant and demonstrating that mice lacking this ISG 15 E1 enzyme were highly susceptible to Sindbis virus infection.
Journal ArticleDOI

Virus-Induced Transient Immune Suppression and the Inhibition of T Cell Proliferation by Type I Interferon

TL;DR: Inhibition of T cell receptor-stimulated bystander CD8 T cell proliferation during acute viral infections may reflect the reduced ability of vaccines to elicit protective immunity when administered during an acute illness.
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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