Interleukin-29 Functions Cooperatively with Interferon to Induce Antiviral Gene Expression and Inhibit Hepatitis C Virus Replication

Pagliaccetti, Nicole E.; Eduardo, Roger; Kleinstein, Steven H.; Mu, Xinmeng Jasmine; Bandi, Prasanthi; Robek, Michael D.

doi:10.1074/jbc.m804296200

Cited by 83 publications

(68 citation statements)

References 53 publications

(68 reference statements)

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“…IFNk/IL-29 shares with type I interferon the same Jak/Stat signalling pathway driving expression of a common set of genes although IFNk/IL-29 binds to a distinct membrane receptor [37]. However, similar to IFNb, IFNk failed to induce S100 gene expression ( Fig.…”

Section: Il-10 and Various Interferones Did Not Alter S100 Gene Exprementioning

confidence: 95%

Double‐stranded RNA induces S100 gene expression by a cycloheximide‐sensitive factor

et al. 2011

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Edited by Hans-Dieter Klenk Keywords:Cytokine burst Non-viral dsRNA Organotypic skin model Secondary response gene Tissue repair a b s t r a c t Viral double-stranded RNA (dsRNA) and its synthetic analog polyI:C are recognized via multiple pathways and induce the expression of genes related to inflammation. In the present study, we demonstrated the polyI:C-induced gene expression of the damage associated molecular pattern (DAMP) molecules S100A8 and S100A9, while other S100 genes were not affected. Cycloheximide and Brefeldin A treatment revealed both the expression of S100A8 and S100A9 as secondary response genes and the involvement of polyI:C-induced cytokines herein. Several type I and type III interferons such as IFNb, IL-20, IL-24, and IFNk/IL-29 were expressed in response to polyI:C, however, they failed to induce S100A8 and S100A9 gene expression. These data indicate the involvement of the danger molecule S100A8/A9 in the resistance against viruses.

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Section: Il-10 and Various Interferones Did Not Alter S100 Gene Exprementioning

confidence: 95%

Double‐stranded RNA induces S100 gene expression by a cycloheximide‐sensitive factor

et al. 2011

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“…Hepatitis C virus could be an important target of IFN-ks, as suggested by genetics studies showing that genetic variation in the gene encoding IFN-k3 predicts hepatitis C treatment-induced viral clearance [110][111][112][113]. Although mouse liver cells might not respond to IFN-ks, it has been shown that IFN-k1 in combination with either IFN-a or IFN-c is able to block hepatitis C virus replication in human hepatocytes, indicating that IFN-ks may be used for treatment of this disease [114].…”

Section: Il-24mentioning

confidence: 99%

Structure and function of interleukin-22 and other members of the interleukin-10 family

Trivella

Ferreira-Junior

Dumoutier

et al. 2010

Cell. Mol. Life Sci.

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The IL-10 family of cytokines is comprised of IL-10, . The IL-10 family members bind to shared class II cytokine receptor chains that associate in various combinations in heterodimeric complexes. Upon interleukin/receptor complex formation, these proteins switch on the Jak/STAT pathway and elicit pleiotropic biological responses whose variety sharply contrasts with their structural similarities. IL-10 family members are involved in several human diseases and health conditions and hence their structural analyses may provide valuable information to design specific therapeutic strategies. In this review, we describe the human interleukin-10 family of cytokines, focusing on their structures and functions, with particular attention given to IL-22 and IL-10. We report on the recently published structures of IL-10 cytokine family members and their complexes with cognate transmembrane and soluble receptors as well as on interleukin physiology and physiopathology.

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“…Therefore, a treatment regimen of both IFN-a and IFN-l might be more promising than the current IFN-a therapy. Pagliaccetti et al reported a cooperative activity of IFN-l1 and IFN-a or IFN-g in inhibiting HCV replication and inducing antiviral gene expression [14]. A Phase Ib clinical trial of IL-29 (IFN-l1) has reported antiviral effects against HCV and low toxicity [15].…”

Section: Impact Of Il-28b Snps On Control Of Hepatitis C Virus Infectmentioning

confidence: 99%

Impact ofIL-28BSNPs on control of hepatitis C virus infection: a genome-wide association study

Imazeki

Yokosuka

Omata

2010

Expert Review of Anti-infective Therapy

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Interleukin-29 Functions Cooperatively with Interferon to Induce Antiviral Gene Expression and Inhibit Hepatitis C Virus Replication

Abstract: The interferon (IFN)-related cytokine interleukin (IL)-

Cited by 83 publications

References 53 publications

Double‐stranded RNA induces S100 gene expression by a cycloheximide‐sensitive factor

Double‐stranded RNA induces S100 gene expression by a cycloheximide‐sensitive factor

Structure and function of interleukin-22 and other members of the interleukin-10 family

Impact ofIL-28BSNPs on control of hepatitis C virus infection: a genome-wide association study

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