Evidence map›Paper›PMID 32353085›Full record

ArticlePLoS pathogens2020

Differential expression of interferon-lambda receptor 1 splice variants determines the magnitude of the antiviral response induced by interferon-lambda 3 in human immune cells.

Deanna M Santer, Gillian E S Minty, Dominic P Golec, Julia Lu, Julia May, Afshin Namdar, Juhi Shah, Shokrollah Elahi, David Proud, Michael Joyce and 2 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

43 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Interferon-JAK-STAT Axis in Bone Metabolism.Current osteoporosis reports · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Mechanisms of Differential Signal Transduction by IFNLR1 Variants.bioRxiv : the preprint server for biology · 2025
    Article
  9. Review
  10. Function of Interferon Lambda Receptor 1 Variants in Stem Cell-Derived Hepatocytes with Abrogated EndogenousJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2025
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Structure-function of type I and III interferons.Current opinion in immunology · 2024
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. DNA-Dependent Interferon Induction and Lung Inflammation inJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2023
    Article
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

12 authors at 2 institutions in 1 country.

Deanna M SanterLi Ka Shing Institute of Virology and Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada.ORCID 0000-0001-6169-7735
Gillian E S MintyLi Ka Shing Institute of Virology and Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada.ORCID 0000-0002-4418-5858
Dominic P GolecAlberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada.
Julia LuLi Ka Shing Institute of Virology and Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada.ORCID 0000-0001-9989-6529
Julia MayLi Ka Shing Institute of Virology and Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada.ORCID 0000-0003-3948-3444
Afshin NamdarLi Ka Shing Institute of Virology and Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada.
Juhi ShahLi Ka Shing Institute of Virology and Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada.ORCID 0000-0002-3552-5873
Shokrollah ElahiLi Ka Shing Institute of Virology and Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada.
David ProudDepartment of Physiology and Pharmacology and Snyder Institute for Chronic Diseases, University of Calgary, Calgary, Alberta, Canada.ORCID 0000-0001-9629-6595
Michael JoyceLi Ka Shing Institute of Virology and Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada.ORCID 0000-0002-9173-7299
D Lorne TyrrellLi Ka Shing Institute of Virology and Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada.ORCID 0000-0002-0983-7267
Michael HoughtonLi Ka Shing Institute of Virology and Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada.ORCID 0000-0003-3762-6771
University of Alberta · CAUniversity of Calgary · CA

Funding

CIHR 353953CIHR 360929
6 · The paper itself

Abstract

Type III interferons (IFN-lambdas(λ)) are important cytokines that inhibit viruses and modulate immune responses by acting through a unique IFN-λR1/IL-10RB heterodimeric receptor. Until now, the primary antiviral function of IFN-λs has been proposed to be at anatomical barrier sites. Here, we examine the regulation of IFN-λR1 expression and measure the downstream effects of IFN-λ3 stimulation in primary human blood immune cells, compared with lung or liver epithelial cells. IFN-λ3 directly bound and upregulated IFN-stimulated gene (ISG) expression in freshly purified human B cells and CD8+ T cells, but not monocytes, neutrophils, natural killer cells, and CD4+ T cells. Despite similar IFNLR1 transcript levels in B cells and lung epithelial cells, lung epithelial cells bound more IFN-λ3, which resulted in a 50-fold greater ISG induction when compared to B cells. The reduced response of B cells could be explained by higher expression of the soluble variant of IFN-λR1 (sIFN-λR1), which significantly reduced ISG induction when added with IFN-λ3 to peripheral blood mononuclear cells or liver epithelial cells. T-cell receptor stimulation potently, and specifically, upregulated membrane-bound IFNLR1 expression in CD4+ T cells, leading to greater antiviral gene induction, and inhibition of human immunodeficiency virus type 1 infection. Collectively, our data demonstrate IFN-λ3 directly interacts with the human adaptive immune system, unlike what has been previously shown in published mouse models, and that type III IFNs could be potentially utilized to suppress both mucosal and blood-borne viral infections.

Indexed as

AnimalsB-LymphocytesCD4-Positive T-LymphocytesCell LineEpithelial CellsGene ExpressionHIV-1HIV InfectionsHumansInterferon alpha-2Interferon LambdaInterferonsInterleukinsLeukocytes, MononuclearLiverLungIFNLR1 protein, humanIFNLR1 protein, mouseInterferon alpha-2Interferon Lambdainterferon-lambda, humanInterferonsInterleukinsReceptors, Interferon

Identifiers

PMID32353085
PMCPMC7217487
OpenAlexW3022536911

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.