Evidence map›Paper›PMID 33212011›Full record

ArticleCell2020

Commensal Microbiota Modulation of Natural Resistance to Virus Infection.

Kailyn L Stefan, Myoungjoo V Kim, Akiko Iwasaki, Dennis L Kasper

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 181 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
181citing papers in PubMed, 2 pooled it
13.1field-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

181 citing papers in PubMed, 2 syntheses or guidelines pooled it, 311 citations in OpenAlex.

  1. Pooled it
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  11. The gut-lung axis in early life: microbiome-associated mechanisms and clinical relevance.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
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  18. Review
  19. Microbiota-dependent IFN-L controls uterine and placental immunity.bioRxiv : the preprint server for biology · 2026
    Article
  20. Article

121 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

4 authors at 3 institutions in 1 country.

Kailyn L StefanDepartment of Immunology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Myoungjoo V KimDepartment of Immunobiology, Yale School of Medicine, New Haven, CT 06510, USA.
Akiko IwasakiDepartment of Immunobiology, Yale School of Medicine, New Haven, CT 06510, USA; Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA.
Dennis L KasperDepartment of Immunology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA. Electronic address: dennis_kasper@hms.harvard.edu.
Harvard University · USHoward Hughes Medical Institute · USYale University · US

Funding

Restimulating memory T cell responses in elderly by a novel, live influenza vaccineR42AI120269 · NIAID · FLUGEN, INC. · PI BILSEL, PAMUK, IWASAKI, AKIKO · 2017 to 2018
$1.8M
Howard Hughes Medical InstituteNIAID NIH HHS R42 AI120269
6 · The paper itself

Abstract

Interferon (IFN)-Is are crucial mediators of antiviral immunity and homeostatic immune system regulation. However, the source of IFN-I signaling under homeostatic conditions is unclear. We discovered that commensal microbes regulate the IFN-I response through induction of IFN-β by colonic DCs. Moreover, the mechanism by which a specific commensal microbe induces IFN-β was identified. Outer membrane (OM)-associated glycolipids of gut commensal microbes belonging to the Bacteroidetes phylum induce expression of IFN-β. Using Bacteroides fragilis and its OM-associated polysaccharide A, we determined that IFN-β expression was induced via TLR4-TRIF signaling. Antiviral activity of this purified microbial molecule against infection with either vesicular stomatitis virus (VSV) or influenza was demonstrated to be dependent on the induction of IFN-β. In a murine VSV infection model, commensal-induced IFN-β regulated natural resistance to virus infection. Due to the physiological importance of IFN-Is, discovery of an IFN-β-inducing microbial molecule represents a potential approach for the treatment of some human diseases.

Indexed as

Immunity, InnateMicrobiotaAnimalsBacteroides fragilisBone Marrow CellsCell MembraneColonDendritic CellsFemaleGene Expression RegulationGlycolipidsInterferon-betaMaleMice, Inbred C57BLPolysaccharides, BacterialToll-Like Receptor 4GlycolipidsInterferon-betaPolysaccharides, BacterialToll-Like Receptor 4Bacteroidesdendritic cellimmune modulationmicrobiometype I interferonvirus infection

Identifiers

PMID33212011
PMCPMC7799371
OpenAlexW3102967988

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.