Evidence map›Paper›PMID 21625574›Full record

ArticlePLoS pathogens2011

Type I interferon production induced by Streptococcus pyogenes-derived nucleic acids is required for host protection.

Nina Gratz, Harald Hartweger, Ulrich Matt, Franz Kratochvill, Marton Janos, Stefanie Sigel, Barbara Drobits, Xiao-Dong Li, Sylvia Knapp, Pavel Kovarik

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
4.8field-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

82 citing papers in PubMed, 125 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. The germ theory revisited: A noncentric view on infection outcome.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  10. Review
  11. Interplay between group AMicrobiology and molecular biology reviews : MMBR · 2024
    Review
  12. Article
  13. 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
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

22 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

10 authors at 5 institutions in 2 countries.

Nina GratzMax F. Perutz Laboratories, Department of Microbiology, Immunobiology and Genetics, University of Vienna, Vienna, Austria.
Harald Hartweger
Ulrich Matt
Franz Kratochvill
Marton Janos
Stefanie Sigel
Barbara Drobits
Xiao-Dong Li
Sylvia Knapp
Pavel Kovarik
Max Perutz Labs · ATMedical University of Vienna · ATUniversity of Vienna · ATCeMM Research Center for Molecular Medicine · ATThe University of Texas Southwestern Medical Center · US

Funding

Austrian Science Fund FWF F 2805Austrian Science Fund FWF I 287
6 · The paper itself

Abstract

Streptococcus pyogenes is a Gram-positive human pathogen that is recognized by yet unknown pattern recognition receptors (PRRs). Engagement of these receptor molecules during infection with S. pyogenes, a largely extracellular bacterium with limited capacity for intracellular survival, causes innate immune cells to produce inflammatory mediators such as TNF, but also type I interferon (IFN). Here we show that signaling elicited by type I IFNs is required for successful defense of mice against lethal subcutaneous cellulitis caused by S. pyogenes. Type I IFN signaling was accompanied with reduced neutrophil recruitment to the site of infection. Mechanistic analysis revealed that macrophages and conventional dendritic cells (cDCs) employ different signaling pathways leading to IFN-beta production. Macrophages required IRF3, STING, TBK1 and partially MyD88, whereas in cDCs the IFN-beta production was fully dependent on IRF5 and MyD88. Furthermore, IFN-beta production by macrophages was dependent on the endosomal delivery of streptococcal DNA, while in cDCs streptococcal RNA was identified as the IFN-beta inducer. Despite a role of MyD88 in both cell types, the known IFN-inducing TLRs were individually not required for generation of the IFN-beta response. These results demonstrate that the innate immune system employs several strategies to efficiently recognize S. pyogenes, a pathogenic bacterium that succeeded in avoiding recognition by the standard arsenal of TLRs.

Indexed as

Dendritic CellsMacrophagesAnimalsCells, CulturedCellulitisDNA, BacterialGene SilencingImmunity, InnateInterferon-betaInterferon Regulatory Factor-3Interferon Regulatory FactorsMembrane ProteinsMiceMice, Inbred C57BLMicroscopy, FluorescenceMyeloid Differentiation Factor 88DNA, BacterialInterferon-betaInterferon Regulatory Factor-3Interferon Regulatory FactorsIrf5 protein, mouseMembrane ProteinsMyd88 protein, mouseMyeloid Differentiation Factor 88Protein Serine-Threonine KinasesReceptors, Pattern RecognitionRNA, BacterialRNA, Small InterferingSting1 protein, mouseSTING ProteinTbk1 protein, mouse

Identifiers

PMID21625574
PMCPMC3098218
OpenAlexW2014105308

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.