Evidence map›Paper›PMID 28953978›Full record

ArticlePLoS pathogens2017

Early IL-6 signalling promotes IL-27 dependent maturation of regulatory T cells in the lungs and resolution of viral immunopathology.

Chloe J Pyle, Faith I Uwadiae, David P Swieboda, James A Harker

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
5.9field-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

82 citing papers in PubMed, 132 citations in OpenAlex.

  1. Trial
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  7. Article
  8. Innate immune role of IL-6 in influenza a virus pathogenesis.Frontiers in cellular and infection microbiology · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Article
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  15. The Mucus-Binding Factor MediatesMicroorganisms · 2024
    Article
  16. Article
  17. Review
  18. ImmunobioticInternational journal of molecular sciences · 2023
    Article
  19. Article
  20. Review

22 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

4 authors at 2 institutions in 1 country.

Chloe J PyleSection of Inflammation, Repair and Development, National Heart and Lung Institute, Imperial College London, South Kensington Campus, South Kensington, London, United Kingdom.ORCID http://orcid.org/0000-0002-1408-1134
Faith I UwadiaeSection of Inflammation, Repair and Development, National Heart and Lung Institute, Imperial College London, South Kensington Campus, South Kensington, London, United Kingdom.ORCID http://orcid.org/0000-0002-6660-6051
David P SwiebodaSection of Inflammation, Repair and Development, National Heart and Lung Institute, Imperial College London, South Kensington Campus, South Kensington, London, United Kingdom.
James A HarkerSection of Inflammation, Repair and Development, National Heart and Lung Institute, Imperial College London, South Kensington Campus, South Kensington, London, United Kingdom.ORCID http://orcid.org/0000-0002-0301-6898
Asthma UK · GBImperial College London · GB

Funding

Medical Research Council G1000758Wellcome Trust
6 · The paper itself

Abstract

Interleukin-6 is a pleiotropic, pro-inflammatory cytokine that can promote both innate and adaptive immune responses. In humans with respiratory virus infections, such as Respiratory Syncytial Virus (RSV), elevated concentrations of IL-6 are associated with more severe disease. In contrast the polymorphisms in the Il6 promoter which favour lower IL-6 production are associated with increased risk of both RSV and Rhinovirus infections. To determine the precise contribution of IL-6 to protection and pathology we used murine models of respiratory virus infection. RSV infection resulted in increased IL-6 production both in the airways and systemically which remained heightened for at least 2 weeks. IL-6 depletion early, but not late, during RSV or Influenza A virus infection resulted in significantly increased disease associated with an influx of virus specific TH1 and cytotoxic CD8+ T cells, whilst not affecting viral clearance. IL-6 acted by driving production of the immunoregulatory cytokine IL-27 by macrophages and monocytes, which in turn promoted the local maturation of regulatory T cells. Concordantly IL-27 was necessary to regulate TH1 responses in the lungs, and sufficient to limit RSV induced disease. Overall we found that during respiratory virus infection the prototypic inflammatory cytokine IL-6 is a critical anti-inflammatory regulator of viral induced immunopathology in the respiratory tract through its induction of IL-27.

Indexed as

Signal TransductionAnimalsInterleukin-6InterleukinsLungMice, Inbred BALB CRespiratory Syncytial Virus InfectionsT-Lymphocytes, RegulatoryIl27 protein, mouseInterleukin-6interleukin-6, mouseInterleukins

Identifiers

PMID28953978
PMCPMC5633202
OpenAlexW2756707886

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.