Evidence map›Paper›PMID 27759022›Full record

ArticleMucosal immunology2017

A critical role for IRF5 in regulating allergic airway inflammation.

A J Byrne, M Weiss, S A Mathie, S A Walker, H L Eames, D Saliba, C M Lloyd, I A Udalova

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

29 citing papers in PubMed, 39 citations in OpenAlex.

  1. Trial
  2. The role of IRF5 as an immune regulator.Biochemical Society transactions · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. IRF3 inhibits nuclear translocation of NF-κB to prevent viral inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  11. Environmental science & technology · 2022
    Article
  12. Review
  13. Article
  14. IRF5 regulates airway macrophage metabolic responses.Clinical and experimental immunology · 2021
    Article
  15. Review
  16. Observational
  17. Article
  18. Article
  19. Article
  20. 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

8 authors at 2 institutions in 1 country.

A J ByrneKennedy Institute of Rheumatology, University of Oxford, Oxford, UK.
M WeissKennedy Institute of Rheumatology, University of Oxford, Oxford, UK.
S A MathieInflammation, Repair & Development Section, National Heart & Lung Institute, Imperial College London, London, UK.
S A WalkerInflammation, Repair & Development Section, National Heart & Lung Institute, Imperial College London, London, UK.
H L EamesKennedy Institute of Rheumatology, University of Oxford, Oxford, UK.
D SalibaKennedy Institute of Rheumatology, University of Oxford, Oxford, UK.
C M LloydInflammation, Repair & Development Section, National Heart & Lung Institute, Imperial College London, London, UK.
I A UdalovaKennedy Institute of Rheumatology, University of Oxford, Oxford, UK.
University of Oxford · GBImperial College London · GB

Funding

Medical Research Council G1000758Versus Arthritis 20892Wellcome TrustWellcome Trust 087618/Z/08/Z
6 · The paper itself

Abstract

Interferon regulatory factor 5 (IRF5) is a key transcription factor involved in the control of the expression of proinflammatory cytokine and responses to infection, but its role in regulating pulmonary immune responses to allergen is unknown. We used genetic ablation, adenoviral vector-driven overexpression, and adoptive transfer approaches to interrogate the role of IRF5 in pulmonary immunity and during challenge with the aeroallergen, house dust mite. Global IRF5 deficiency resulted in impaired lung function and extracellular matrix (ECM) deposition. IRF5 was also essential for effective responses to inhaled allergen, controlling airway hyperresponsiveness, mucus secretion, and eosinophilic inflammation. Adoptive transfer of IRF5-deficient alveolar macrophages into the wild-type pulmonary milieu was sufficient to drive airway hyperreactivity, at baseline or following antigen challenge. These data identify IRF5-expressing macrophages as a key component of the immune defense of the airways. Manipulation of IRF5 activity in the lung could therefore be a viable strategy for the redirection of pulmonary immune responses and, thus, the treatment of lung disorders.

Indexed as

Adoptive TransferAnimalsAntigens, DermatophagoidesCell MovementCells, CulturedEosinophilsExtracellular MatrixFemaleHypersensitivityInterferon Regulatory FactorsLungMacrophages, AlveolarMiceMice, Inbred C57BLMice, KnockoutMucusAntigens, DermatophagoidesInterferon Regulatory FactorsIrf5 protein, mouse

Identifiers

PMID27759022
PMCPMC5266556
OpenAlexW2537956131

What OpenQuestion holds

Textmetadata
LicenceTDM
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.