Evidence map›Paper›PMID 27811478›Full record

ArticleJournal of innate immunity2017

Deletion of Irf3 and Irf7 Genes in Mice Results in Altered Interferon Pathway Activation and Granulocyte-Dominated Inflammatory Responses to Influenza A Infection.

Bastian Hatesuer, Hang Thi Thu Hoang, Peggy Riese, Stephanie Trittel, Ingo Gerhauser, Husni Elbahesh, Robert Geffers, Esther Wilk, Klaus Schughart

Open access · goldAbstract read
In one paragraph

Article in Journal of innate immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Cellular nucleic acid-binding protein is essential for type I interferon-mediated immunity to RNA virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  20. TBK1 recruitment to STING activates both IRF3 and NF-κB that mediate immune defense against tumors and viral infections.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
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

9 authors at 4 institutions in 3 countries.

Bastian HatesuerDepartment of Infection Genetics, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Hang Thi Thu Hoang
Peggy Riese
Stephanie Trittel
Ingo Gerhauser
Husni Elbahesh
Robert Geffers
Esther Wilk
Klaus Schughart
Biology of Infection · FRHelmholtz Centre for Infection Research · DEUniversity of Tennessee Health Science Center · USUniversity of Veterinary Medicine Hannover, Foundation · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The interferon (IFN) pathway plays an essential role in the innate immune response following viral infections and subsequent shaping of adaptive immunity. Infections with influenza A viruses (IAV) activate the IFN pathway after the recognition of pathogen-specific molecular patterns by respective pattern recognition receptors. The IFN regulatory factors IRF3 and IRF7 are key players in the regulation of type I and III IFN genes. In this study, we analyzed the role of IRF3 and IRF7 for the host response to IAV infections in Irf3-/-, Irf7-/-, and Irf3-/-Irf7-/- knockout mice. While the absence of IRF3 had only a moderate impact on IFN expression, deletion of IRF7 completely abolished IFNα production after infection. In contrast, lack of both IRF3 and IRF7 resulted in the absence of both IFNα and IFNβ after IAV infection. In addition, IAV infection of double knockout mice resulted in a strong increase of mortality associated with a massive influx of granulocytes in the lung and reduced activation of the adaptive immune response.

Indexed as

Adaptive ImmunityAnimalsCells, CulturedGranulocytesInflammationInfluenza A virusInterferon-alphaInterferon Regulatory Factor-3Interferon Regulatory Factor-7LungMiceMice, Inbred C57BLMice, KnockoutOrthomyxoviridae InfectionsSignal TransductionInterferon-alphaInterferon Regulatory Factor-3Interferon Regulatory Factor-7Irf3 protein, mouseIrf7 protein, mouse

Identifiers

PMID27811478
PMCPMC6738875
OpenAlexW2547765422

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.