Evidence map›Paper›PMID 18787692›Full record

ArticlePLoS pathogens2008

Interferon-lambda contributes to innate immunity of mice against influenza A virus but not against hepatotropic viruses.

Markus Mordstein, Georg Kochs, Laure Dumoutier, Jean-Christophe Renauld, Søren R Paludan, Kevin Klucher, Peter Staeheli

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 212 papers.

0numbers the graph read from it
0cells of the map it votes in
212citing papers in PubMed
11.2field-weighted citation impact, top 1% 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

212 citing papers in PubMed, 317 citations in OpenAlex.

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  10. Exploiting a type III interferon response to improve chemotherapeutic safety and efficacy.European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences · 2025
    Article
  11. Article
  12. Interferon lambda 4 is a gut antimicrobial protein.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Meeting the Challenge of Controlling Viral Immunopathology.International journal of molecular sciences · 2024
    Review
  19. Article
  20. Article

152 more citing papers are in PubMed but not listed here.

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

7 authors at 3 institutions in 3 countries.

Markus MordsteinDepartment of Virology, University of Freiburg, Freiburg, Germany.
Georg Kochs
Laure Dumoutier
Jean-Christophe Renauld
Søren R Paludan
Kevin Klucher
Peter Staeheli
University of Freiburg · DELudwig Cancer Research · BEAarhus University · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Virus-infected cells secrete a broad range of interferon (IFN) subtypes which in turn trigger the synthesis of antiviral factors that confer host resistance. IFN-alpha, IFN-beta and other type I IFNs signal through a common universally expressed cell surface receptor, whereas IFN-lambda uses a distinct receptor complex for signaling that is not present on all cell types. Since type I IFN receptor-deficient mice (IFNAR1(0/0)) exhibit greatly increased susceptibility to various viral diseases, it remained unclear to which degree IFN-lambda might contribute to innate immunity. To address this issue we performed influenza A virus infections of mice which carry functional alleles of the influenza virus resistance gene Mx1 and which, therefore, develop a more complete innate immune response to influenza viruses than standard laboratory mice. We demonstrate that intranasal administration of IFN-lambda readily induced the antiviral factor Mx1 in mouse lungs and efficiently protected IFNAR1(0/0) mice from lethal influenza virus infection. By contrast, intraperitoneal application of IFN-lambda failed to induce Mx1 in the liver of IFNAR1(0/0) mice and did not protect against hepatotropic virus infections. Mice lacking functional IFN-lambda receptors were only slightly more susceptible to influenza virus than wild-type mice. However, mice lacking functional receptors for both IFN-alpha/beta and IFN-lambda were hypersensitive and even failed to restrict usually non-pathogenic influenza virus mutants lacking the IFN-antagonistic factor NS1. Interestingly, the double-knockout mice were not more susceptible against hepatotropic viruses than IFNAR1(0/0) mice. From these results we conclude that IFN-lambda contributes to inborn resistance against viral pathogens infecting the lung but not the liver.

Indexed as

AnimalsCytokinesGTP-Binding ProteinsHepatovirusImmunity, InnateInfluenza A virusInterferon LambdaInterleukinsLungMiceMice, KnockoutMyxovirus Resistance ProteinsOrthomyxoviridae InfectionsReceptors, InterferonCytokinesGTP-Binding ProteinsInterferon Lambdainterferon-lambda protein, mouseInterleukinsMx1 protein, mouseMyxovirus Resistance ProteinsReceptors, Interferon

Identifiers

PMID18787692
PMCPMC2522277
OpenAlexW2006328907

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.