Evidence map›Paper›PMID 32527928›Full record

ArticleScience (New York, N.Y.)2020

Type I and III interferons disrupt lung epithelial repair during recovery from viral infection.

Jack Major, Stefania Crotta, Miriam Llorian, Teresa M McCabe, Hans Henrik Gad, Simon L Priestnall, Rune Hartmann, Andreas Wack

Open access · hybridAbstract read
In one paragraph

Article in Science (New York, N.Y.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 348 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
348citing papers in PubMed, 1 pooled it
49.3field-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

348 citing papers in PubMed, 1 synthesis or guideline pooled it, 494 citations in OpenAlex.

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  11. Mapping the dialogue: Decoding alveolar stem-niche interactions.Proceedings of the National Academy of Sciences of the United States of America · 2026
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288 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Jack MajorImmunoregulation Laboratory, The Francis Crick Institute, London, UK.ORCID 0000-0002-8018-1512
Stefania CrottaImmunoregulation Laboratory, The Francis Crick Institute, London, UK.ORCID 0000-0003-4676-8616
Miriam LlorianBioinformatics and Biostatistics, The Francis Crick Institute, London, UK.
Teresa M McCabeImmunoregulation Laboratory, The Francis Crick Institute, London, UK.ORCID 0000-0003-0083-6310
Hans Henrik GadDepartment of Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark.ORCID 0000-0001-8449-1115
Simon L PriestnallDepartment of Pathobiology and Population Sciences, The Royal Veterinary College, Hatfield, UK.
Rune HartmannDepartment of Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark.ORCID 0000-0003-1159-066X
Andreas WackImmunoregulation Laboratory, The Francis Crick Institute, London, UK. andreas.wack@crick.ac.uk.ORCID 0000-0001-5226-2991
The Francis Crick Institute · GBAarhus University · DKRoyal Veterinary College · GB

Funding

Cancer Research UK FC001206Wellcome Trust FC001206
6 · The paper itself

Abstract

Excessive cytokine signaling frequently exacerbates lung tissue damage during respiratory viral infection. Type I (IFN-α and IFN-β) and III (IFN-λ) interferons are host-produced antiviral cytokines. Prolonged IFN-α and IFN-β responses can lead to harmful proinflammatory effects, whereas IFN-λ mainly signals in epithelia, thereby inducing localized antiviral immunity. In this work, we show that IFN signaling interferes with lung repair during influenza recovery in mice, with IFN-λ driving these effects most potently. IFN-induced protein p53 directly reduces epithelial proliferation and differentiation, which increases disease severity and susceptibility to bacterial superinfections. Thus, excessive or prolonged IFN production aggravates viral infection by impairing lung epithelial regeneration. Timing and duration are therefore critical parameters of endogenous IFN action and should be considered carefully for IFN therapeutic strategies against viral infections such as influenza and coronavirus disease 2019 (COVID-19).

Indexed as

Alveolar Epithelial CellsAnimalsApoptosisBronchoalveolar Lavage FluidCell DifferentiationCell ProliferationCells, CulturedCytokinesFemaleInfluenza A Virus, H3N2 SubtypeInterferon-alphaInterferon-betaInterferon LambdaInterferonsInterferon Type IInterleukinsCytokinesIFNLR1 protein, mouseInterferon-alphaInterferon-betaInterferon Lambdainterferon-lambda protein, mouseInterferonsInterferon Type IInterleukinsReceptor, Interferon alpha-betaReceptors, InterferonTrp53 protein, mouseTumor Suppressor Protein p53

Identifiers

PMID32527928
PMCPMC7292500
OpenAlexW3035343971

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.