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Open AccessJournal ArticleDOI

Distinct Poly(I-C) and Virus-activated Signaling Pathways Leading to Interferon-β Production in Hepatocytes

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TLDR
It is concluded that hepatocytes contain two distinct antiviral signaling pathways leading to expression of type I IFNs, one dependent upon TLR3 and the other dependent on RIG-I, with little cross-talk between these pathways.
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This article is published in Journal of Biological Chemistry.The article was published on 2005-04-29 and is currently open access. It has received 371 citations till now. The article focuses on the topics: Interferon & Interferon inducer.

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Journal ArticleDOI

Evasion of intracellular host defence by hepatitis C virus

TL;DR: Hepatitis C virus evades the host response through a complex combination of processes that include signalling interference, effector modulation and continual viral genetic variation.
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The RNA Helicase Lgp2 Inhibits TLR-Independent Sensing of Viral Replication by Retinoic Acid-Inducible Gene-I

TL;DR: It is proposed that Lgp2 acts as a negative feedback regulator of antiviral signaling by sequestering dsRNA from RIG-I, and inhibits SV and Newcastle disease virus signaling to IFN-stimulated regulatory element- and NF-κB-dependent pathways.
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Toll-like receptors in antiviral innate immunity

TL;DR: The current knowledge of the roles TLRs play in antiviral innate immune responses is reviewed, examples of TLR-mediated viral recognition are discussed, and strategies used by viruses to antagonize the host antiviral inherent immune responses are described.
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Toll-like receptor signaling in the liver.

TL;DR: There is still a fundamental lack of knowledge about the functional expression of TLR and TLR adapter molecules in the liver under normal and pathological conditions and future studies need to further investigate the role of TLRs in hepatic fibrogenesis and characterize the “good” signals induced by TLR.
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Activation of the mammalian immune system by siRNAs.

TL;DR: The application of screening assays for nonspecific activation of both innate and acquired immunity will be necessary for further development of RNAi as a therapeutic tool.
References
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Journal ArticleDOI

Recognition of double-stranded RNA and activation of NF-kappaB by Toll-like receptor 3.

TL;DR: It is shown that mammalian TLR3 recognizes dsRNA, and that activation of the receptor induces the activation of NF-κB and the production of type I interferons (IFNs).
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Toll-like receptor control of the adaptive immune responses.

TL;DR: Recognition of microbial infection and initiation of host defense responses is controlled by multiple mechanisms and recent studies have provided important clues about the mechanisms of TLR-mediated control of adaptive immunity orchestrated by dendritic cell populations in distinct anatomical locations.
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Species-Specific Recognition of Single-Stranded RNA via Toll-like Receptor 7 and 8

TL;DR: It is shown that guanosine (G)- and uridine (U)-rich ssRNA oligonucleotides derived from human immunodeficiency virus–1 (HIV-1) stimulate dendritic cells and macrophages to secrete interferon-α and proinflammatory, as well as regulatory, cytokines, and these data suggest that ssRNA represents a physiological ligand for TLR7 and TLR8.
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The RNA helicase RIG-I has an essential function in double-stranded RNA-induced innate antiviral responses.

TL;DR: In this article, the authors identify retinoic acid inducible gene I (RIG-I), which encodes a DExD/H box RNA helicase that contains a caspase recruitment domain, as an essential regulator for dsRNA-induced signaling.
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Innate antiviral responses by means of TLR7-mediated recognition of single-stranded RNA.

TL;DR: These results identify ssRNA as a ligand for TLR7 and suggest that cells of the innate immune system sense endosomal ssRNA to detect infection by RNA viruses.
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