Evidence map›Paper›PMID 18757365›Full record

ArticleThe Journal of biological chemistry2008

Interleukin-29 functions cooperatively with interferon to induce antiviral gene expression and inhibit hepatitis C virus replication.

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

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
6.1field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

43 citing papers in PubMed, 94 citations in OpenAlex.

  1. Article
  2. Review
  3. Mechanisms of Innate Immune Activation by a Hybrid Alphavirus-Rhabdovirus Vaccine Platform.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2020
    Article
  4. Article
  5. Dexamethasone decreases IL-29 expression in house dust mite-stimulated human bronchial epithelial cells.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2015
    Article
  6. Kinetic Differences and Synergistic Antiviral Effects Between Type I and Type III Interferon Signaling Indicate Pathway Independence.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2015
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Nicole E PagliaccettiDepartment of Pathology, Yale University School of Medicine, New Haven, Connecticut 06510, USA.
Roger Eduardo
Steven H Kleinstein
Xinmeng Jasmine Mu
Prasanthi Bandi
Michael D Robek
Yale University · US

Funding

Viral Pathogenesis and TherapeuticsU54AI057158 · NIAID · WADSWORTH CENTER · PI LEVY, DAVID E · 2003 to 2014
$100.8M
Predoctoral Training Program in VirologyT32AI055403 · NIAID · YALE UNIVERSITY · PI KUMAR, PRITI, MOTHES, WALTHER H · 2003 to 2024
$3.6M
Modulation of HBV Replication by the ImmunoproteasomeK22AI064757 · NIAID · YALE UNIVERSITY · PI ROBEK, MICHAEL D · 2005 to 2006
$268k
NIAID NIH HHS AI055403NIAID NIH HHS K22 AI064757NIAID NIH HHS U54-AI057158
6 · The paper itself

Abstract

The interferon (IFN)-related cytokine interleukin (IL)-29 (also known as IFN-lambda1) inhibits virus replication by inducing a cellular antiviral response similar to that activated by IFN-alpha/beta. However, because it binds to a unique receptor, this cytokine may function cooperatively with IFN-alpha/beta or IFN-gamma during natural infections to inhibit virus replication, and might also be useful therapeutically in combination with other cytokines to treat chronic viral infections such as hepatitis C (HCV). We therefore investigated the ability of IL-29 and IFN-alpha or IFN-gamma to cooperatively inhibit virus replication and induce antiviral gene expression. Compared with the individual cytokines alone, the combination of IL-29 with IFN-alpha or IFN-gamma was more effective at blocking vesicular stomatitis virus and HCV replication, and this cooperative antiviral activity correlated with the magnitude of induced antiviral gene expression. Although the combined effects of IL-29 and IFN-alpha were primarily additive, the IL-29/IFN-gamma combination synergistically induced multiple genes and had the greatest antiviral activity. Two different mechanisms contributed to the enhanced gene expression induced by the cytokine combinations: increased activation of ISRE promoter elements and simultaneous activation of both ISRE and GAS elements within the same promoter. These findings provide new insight into the coregulation of a critical innate immune response by functionally distinct cytokine families.

Indexed as

Gene Expression RegulationAntiviral AgentsBase SequenceCell Line, TumorCell ProliferationCell SurvivalGene Expression ProfilingHepacivirusHepatitis CHumansInterferon LambdaInterferonsInterleukinsModels, BiologicalMolecular Sequence DataPromoter Regions, GeneticAntiviral AgentsInterferon Lambdainterferon-lambda, humanInterferonsInterleukins

Identifiers

PMID18757365
PMCPMC2662072
OpenAlexW2045882981

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.