Evidence map›Paper›PMID 25614319›Full record

ReviewNature reviews. Immunology2015

Type I interferons in infectious disease.

Finlay McNab, Katrin Mayer-Barber, Alan Sher, Andreas Wack, Anne O'Garra

Open access · bronzeAbstract readReview
In one paragraph

Review in Nature reviews. Immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,774 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,774citing papers in PubMed, 2 pooled it
67.7field-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

1,774 citing papers in PubMed, 2 syntheses or guidelines pooled it, 2,694 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Gut microbes · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Trimethylamine-N-oxide: the microbial cue in immune-mediated disorders.Trends in endocrinology and metabolism: TEM · 2026
    Review
  13. Article
  14. IFN-κ directs antiviral immunity in human skin.bioRxiv : the preprint server for biology · 2026
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Powassan Virus NS5 Antagonizes TYK2-Mediated Immune Signaling Pathways.bioRxiv : the preprint server for biology · 2026
    Article
  20. Review

1,714 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

5 authors at 4 institutions in 2 countries.

Finlay McNab1] Allergic Inflammation Discovery Performance Unit, Respiratory Disease Respiratory Research and Development, GlaxoSmithKline, Stevenage, Hertfordshire SG1 2NY, UK. [2] Division of Immunoregulation, Medical Research Council (MRC) National Institute for Medical Research, Mill Hill, London NW7 1AA, UK.
Katrin Mayer-BarberImmunobiology Section, Laboratory of Parasitic Diseases (LPD), National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Maryland 20892, USA.
Alan SherImmunobiology Section, Laboratory of Parasitic Diseases (LPD), National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Maryland 20892, USA.
Andreas WackDivision of Immunoregulation, Medical Research Council (MRC) National Institute for Medical Research, Mill Hill, London NW7 1AA, UK.
Anne O'Garra1] Division of Immunoregulation, Medical Research Council (MRC) National Institute for Medical Research, Mill Hill, London NW7 1AA, UK. [2] National Heart and Lung Institute (NHLI), Faculty of Medicine, Imperial College London, London, UK.
Medical Research Council · GBImperial College London · GBNational Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

Innate inflammatory responses during pulmonary infectionsZIAAI001207 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MAYER-BARBER, KATRIN · 2015 to 2025
$13.6M
Innate Determinants of Microbial ImmunityZIAAI001044 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SHER, ALAN · 2009 to 2022
$8.8M
Cancer Research UK FC001126Medical Research Council MC_U117565642Medical Research Council MC_U117597139Medical Research Council U117565642Medical Research Council U117597139
6 · The paper itself

Abstract

Type I interferons (IFNs) have diverse effects on innate and adaptive immune cells during infection with viruses, bacteria, parasites and fungi, directly and/or indirectly through the induction of other mediators. Type I IFNs are important for host defence against viruses. However, recently, they have been shown to cause immunopathology in some acute viral infections, such as influenza virus infection. Conversely, they can lead to immunosuppression during chronic viral infections, such as lymphocytic choriomeningitis virus infection. During bacterial infections, low levels of type I IFNs may be required at an early stage, to initiate cell-mediated immune responses. High concentrations of type I IFNs may block B cell responses or lead to the production of immunosuppressive molecules, and such concentrations also reduce the responsiveness of macrophages to activation by IFNγ, as has been shown for infections with Listeria monocytogenes and Mycobacterium tuberculosis. Recent studies in experimental models of tuberculosis have demonstrated that prostaglandin E2 and interleukin-1 inhibit type I IFN expression and its downstream effects, demonstrating that a cross-regulatory network of cytokines operates during infectious diseases to provide protection with minimum damage to the host.

Indexed as

AnimalsBacterial InfectionsCommunicable DiseasesHumansInterferon Type IMycosesParasitic DiseasesSignal TransductionVirus DiseasesInterferon Type I

Identifiers

PMID25614319
PMCPMC7162685
OpenAlexW2091129202

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.