Evidence map›Paper›PMID 32977999›Full record

ReviewTrends in genetics : TIG2021

Genetic Lesions of Type I Interferon Signalling in Human Antiviral Immunity.

Christopher J A Duncan, Richard E Randall, Sophie Hambleton

Open access · hybridAbstract readReview
In one paragraph

Review in Trends in genetics : TIG, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

63 citing papers in PubMed, 95 citations in OpenAlex.

  1. Review
  2. Article
  3. Inflammasomes in Sjögren's Disease: Exploring the Therapeutic Value.International journal of molecular sciences · 2026
    Review
  4. Article
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  20. Infections in Inborn Errors of STATs.Pathogens (Basel, Switzerland) · 2024
    Review

3 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

3 authors at 2 institutions in 1 country.

Christopher J A DuncanTranslational and Clinical Research Institute, Immunity and Inflammation Theme, Newcastle University, Newcastle upon Tyne NE2 4HH, UK; Royal Victoria Infirmary, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne NE1 4LP, UK. Electronic address: christopher.duncan@ncl.ac.uk.
Richard E RandallSchool of Biology, University of St Andrew's, St Andrew's KY16 9ST, UK.
Sophie HambletonTranslational and Clinical Research Institute, Immunity and Inflammation Theme, Newcastle University, Newcastle upon Tyne NE2 4HH, UK; Great North Children's Hospital, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne NE1 4LP, UK.
Newcastle upon Tyne Hospitals NHS Foundation Trust · GBUniversity of St Andrews · GB

Funding

Wellcome Trust 207556/Z/17/ZWellcome Trust 211153/Z/18/Z
6 · The paper itself

Abstract

The concept that type I interferons (IFN-I) are essential to antiviral immunity derives from studies on animal models and cell lines. Virtually all pathogenic viruses have evolved countermeasures to IFN-I restriction, and genetic loss of viral IFN-I antagonists leads to virus attenuation. But just how important is IFN-I to antiviral defence in humans? The recent discovery of genetic defects of IFN-I signalling illuminates this and other questions of IFN biology, including the role of the mucosa-restricted type III IFNs (IFN-III), informing our understanding of the place of the IFN system within the concerted antiviral response. Here we review monogenic lesions of IFN-I signalling pathways and summarise the organising principles which emerge.

Indexed as

AnimalsHumansImmunity, InnateInterferon Type ISignal TransductionVirusesInterferon Type Iantiviral immunityIFNARinborn errors of immunityinterferon-stimulated genesJAK–STAT signallingtype I interferons

Identifiers

PMID32977999
PMCPMC7508017
OpenAlexW3088819025

What OpenQuestion holds

Textmetadata
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.