Evidence map›Paper›PMID 27520969›Full record

ArticleEMBO molecular medicine2016

IFNλ is a potent anti-influenza therapeutic without the inflammatory side effects of IFNα treatment.

Sophia Davidson, Teresa M McCabe, Stefania Crotta, Hans Henrik Gad, Edith M Hessel, Soren Beinke, Rune Hartmann, Andreas Wack

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 179 papers.

0numbers the graph read from it
0cells of the map it votes in
179citing papers in PubMed
7.6field-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.

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

179 citing papers in PubMed, 238 citations in OpenAlex.

  1. Early Treatment with Pegylated Interferon Lambda for Covid-19.The New England journal of medicine · 2023
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  15. Interferon-JAK-STAT Axis in Bone Metabolism.Current osteoporosis reports · 2026
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. βNature communications · 2025
    Article

119 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

8 authors at 3 institutions in 2 countries.

Sophia DavidsonImmunoregulation Laboratory, Mill Hill Laboratory, Francis Crick Institute, London, UK.
Teresa M McCabeImmunoregulation Laboratory, Mill Hill Laboratory, Francis Crick Institute, London, UK.ORCID 0000-0002-0298-1426
Stefania CrottaImmunoregulation Laboratory, Mill Hill Laboratory, Francis Crick Institute, London, UK.ORCID 0000-0003-4676-8616
Hans Henrik GadDepartment of Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark.
Edith M HesselRefractory Respiratory Inflammation Discovery Performance Unit, Respiratory Therapy Area, GSK, Stevenage, UK.
Soren BeinkeRefractory Respiratory Inflammation Discovery Performance Unit, Respiratory Therapy Area, GSK, Stevenage, UK.ORCID 0000-0002-2850-5241
Rune HartmannDepartment of Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark.ORCID 0000-0003-1159-066X
Andreas WackImmunoregulation Laboratory, Mill Hill Laboratory, Francis Crick Institute, London, UK andreas.wack@crick.ac.uk.ORCID 0000-0001-5226-2991
The Francis Crick Institute · GBAarhus University · DKAge UK · GB

Funding

Biotechnology and Biological Sciences Research Council BB/K501475/1Cancer Research UKMedical Research Council MC_U117597139Medical Research Council U117597139Wellcome Trust
6 · The paper itself

Abstract

Influenza A virus (IAV)-induced severe disease is characterized by infected lung epithelia, robust inflammatory responses and acute lung injury. Since type I interferon (IFNαβ) and type III interferon (IFNλ) are potent antiviral cytokines with immunomodulatory potential, we assessed their efficacy as IAV treatments. IFNλ treatment of IAV-infected Mx1-positive mice lowered viral load and protected from disease. IFNα treatment also restricted IAV replication but exacerbated disease. IFNα treatment increased pulmonary proinflammatory cytokine secretion, innate cell recruitment and epithelial cell death, unlike IFNλ-treatment. IFNλ lacked the direct stimulatory activity of IFNα on immune cells. In epithelia, both IFNs induced antiviral genes but no inflammatory cytokines. Similarly, human airway epithelia responded to both IFNα and IFNλ by induction of antiviral genes but not of cytokines, while hPBMCs responded only to IFNα. The restriction of both IFNλ responsiveness and productive IAV replication to pulmonary epithelia allows IFNλ to limit IAV spread through antiviral gene induction in relevant cells without overstimulating the immune system and driving immunopathology. We propose IFNλ as a non-inflammatory and hence superior treatment option for human IAV infection.

Indexed as

AnimalsCell DeathCytokinesDisease Models, AnimalEpithelial CellsHumansInfluenza A virusInterferon-alphaInterferon LambdaInterleukinsLeukocytesLungMiceOrthomyxoviridae InfectionsTreatment OutcomeViral LoadCytokinesIFNL4 protein, humanInterferon-alphaInterferon LambdaInterleukinsimmunopathologyinfectioninfluenzainterferon alphainterferon lambda

Identifiers

PMID27520969
PMCPMC5009813
OpenAlexW2517547699

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.