Evidence map›Paper›PMID 25941255›Full record

ArticleThe Journal of experimental medicine2015

IFN-λ resolves inflammation via suppression of neutrophil infiltration and IL-1β production.

Katrina Blazek, Hayley L Eames, Miriam Weiss, Adam J Byrne, Dany Perocheau, James E Pease, Sean Doyle, Fiona McCann, Richard O Williams, Irina A Udalova

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02498808 (Interferon-lambda), which is not on this map. Cited by 140 papers.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed
8.0field-weighted citation impact, top 2% 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.

NCT02498808 unknown statusnot on this map

Interferon-lambda: Novel Biologics for Controlling Neutrophil-mediated Pathology in Rheumatic Diseases?

TypeobservationalSponsorUniversity of OxfordRan2015 to 2018Enrolled85ConditionsArthritis, Vasculitis
3 · Its place in the literature

Who cites it

140 citing papers in PubMed, 213 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Interferon-JAK-STAT Axis in Bone Metabolism.Current osteoporosis reports · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Interferon Lambda: The Next Frontier in Antiviral Therapy?Pharmaceuticals (Basel, Switzerland) · 2025
    Review
  11. Article
  12. Review
  13. Review
  14. 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
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Katrina BlazekKennedy Institute of Rheumatology, University of Oxford, Oxford OX3 7HE, England, UK.
Hayley L EamesKennedy Institute of Rheumatology, University of Oxford, Oxford OX3 7HE, England, UK.
Miriam WeissKennedy Institute of Rheumatology, University of Oxford, Oxford OX3 7HE, England, UK.
Adam J ByrneKennedy Institute of Rheumatology, University of Oxford, Oxford OX3 7HE, England, UK.
Dany PerocheauKennedy Institute of Rheumatology, University of Oxford, Oxford OX3 7HE, England, UK.
James E PeaseNational Heart and Lung Institute, Imperial College London, London SW7 2AZ, England, UK.
Sean DoyleZymoGenetics, Inc., Seattle, WA 98109.
Fiona McCannKennedy Institute of Rheumatology, University of Oxford, Oxford OX3 7HE, England, UK.
Richard O WilliamsKennedy Institute of Rheumatology, University of Oxford, Oxford OX3 7HE, England, UK.
Irina A UdalovaKennedy Institute of Rheumatology, University of Oxford, Oxford OX3 7HE, England, UK irina.udalova@kennedy.ox.ac.uk.
University of Oxford · GBImperial College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The most studied biological role of type III interferons (IFNs) has so far been their antiviral activity, but their role in autoimmune and inflammatory diseases remains largely unexplored. Here, we show that treatment with IFN-λ2/IL-28A completely halts and reverses the development of collagen-induced arthritis (CIA) and discover cellular and molecular mechanisms of IL-28A antiinflammatory function. We demonstrate that treatment with IL-28A dramatically reduces numbers of proinflammatory IL-17-producing Th17 and γδ T cells in the joints and inguinal lymph nodes, without affecting T cell proliferative responses or levels of anticollagen antibodies. IL-28A exerts its antiinflammatory effect by restricting recruitment of IL-1b-expressing neutrophils, which are important for amplification of inflammation. We identify neutrophils as cells expressing high levels of IFN-λ receptor 1 (IFNLR1)-IL-28 receptor α (IL28RA) and targeted by IL-28A. Our data highlight neutrophils as contributors to the pathogenesis of autoimmune arthritis and present IFN-λs or agonists of IFNLR1-IL28RA as putative new therapeutics for neutrophil-driven inflammation.

Indexed as

Gene Expression RegulationAnimalsArthritisCattleCD4-Positive T-LymphocytesCell MovementCell ProliferationChickensCollagenFlow CytometryInflammationInterferon LambdaInterleukin-17Interleukin-1betaInterleukinsMaleCollagenIL28A protein, mouseInterferon LambdaInterleukin-17Interleukin-1betainterleukin 28alpha receptorInterleukinsReceptors, Antigen, T-Cell, gamma-deltaReceptors, Cytokine

Identifiers

PMID25941255
PMCPMC4451128
OpenAlexW2209458064

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

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.