Evidence map›Paper›PMID 20478539›Full record

ArticleCell host & microbe2010

A Yersinia effector protein promotes virulence by preventing inflammasome recognition of the type III secretion system.

Igor E Brodsky, Noah W Palm, Saheli Sadanand, Michelle B Ryndak, Fayyaz S Sutterwala, Richard A Flavell, James B Bliska, Ruslan Medzhitov

Open access · bronzeAbstract read
In one paragraph

Article in Cell host & microbe, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 174 papers.

0numbers the graph read from it
0cells of the map it votes in
174citing papers in PubMed
16.3field-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

174 citing papers in PubMed, 303 citations in OpenAlex.

  1. Article
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  9. Current Challenges inMicroorganisms · 2025
    Review
  10. Article
  11. Article
  12. Review
  13. TLR priming licenses NAIP inflammasome activation by immunoevasive ligands.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Distinct Mechanisms of Type 3 Secretion System Recognition Control LTBbioRxiv : the preprint server for biology · 2024
    Article
  20. Review

114 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 4 institutions in 1 country.

Igor E BrodskyDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA. igor.brodsky@yale.edu
Noah W Palm
Saheli Sadanand
Michelle B Ryndak
Fayyaz S Sutterwala
Richard A Flavell
James B Bliska
Ruslan Medzhitov
Yale University · USHoward Hughes Medical Institute · USStony Brook University · USUniversity of Iowa · US

Funding

Treatments for Nipah Virus InfectionU54AI057159 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WHELAN, SEAN PJ · 2003 to 2013
$113.7M
Viral Pathogenesis and TherapeuticsU54AI057158 · NIAID · WADSWORTH CENTER · PI LEVY, DAVID E · 2003 to 2014
$100.8M
Toll Pathway & Control of Adaptive Immune ResponsesR01AI055502 · NIAID · YALE UNIVERSITY · PI MEDZHITOV, RUSLAN · 2003 to 2013
$3.7M
MODULATION OF HOST SIGNALING FUNCTIONS BY YERSINIA YOPSR01AI043389 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI BLISKA, JAMES B · 2000 to 2009
$3.1M
Interaction of Yersinia with dendritic cellsF32AI065081 · NIAID · YALE UNIVERSITY · PI BRODSKY, IGOR E · 2005 to 2007
$143k
Howard Hughes Medical InstituteNIAID NIH HHS F32 AI065081NIAID NIH HHS R01 AI043389NIAID NIH HHS R01 AI055502NIAID NIH HHS RCE AI057159NIAID NIH HHS U54 AI057158NIAID NIH HHS U54-AI057158NIAID NIH HHS U54 AI057159
6 · The paper itself

Abstract

Bacterial pathogens utilize pore-forming toxins or specialized secretion systems to deliver virulence factors to modulate host cell physiology and promote bacterial replication. Detection of these secretion systems or toxins, or their activities, by nucleotide-binding oligomerization domain leucine-rich repeat proteins (NLRs) triggers the assembly of inflammasomes, multiprotein complexes necessary for caspase-1 activation and host defense. Here we demonstrate that caspase-1 activation in response to the Yersinia type III secretion system (T3SS) requires the adaptor ASC and involves both NLRP3 and NLRC4 inflammasomes. Further, we identify a Yersinia type III secreted effector protein, YopK, which interacts with the T3SS translocon to prevent cellular recognition of the T3SS and inflammasome activation. In the absence of YopK, inflammasome sensing of the T3SS promotes bacterial clearance from infected tissues in vivo. These data demonstrate that a class of bacterial proteins interferes with cellular recognition of bacterial secretion systems and contributes to bacterial survival within host tissues.

Indexed as

Immune EvasionAnimalsBacterial ProteinsCalcium-Binding ProteinsCARD Signaling Adaptor ProteinsCarrier ProteinsCaspase 1Cells, CulturedCell SurvivalMembrane Transport ProteinsMiceMice, KnockoutModels, BiologicalNLR Family, Pyrin Domain-Containing 3 ProteinVirulenceVirulence FactorsBacterial ProteinsCalcium-Binding ProteinsCARD Signaling Adaptor ProteinsCarrier ProteinsCaspase 1Membrane Transport ProteinsNLRC4 protein, humanNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanVirulence Factors

Identifiers

PMID20478539
PMCPMC2883865
OpenAlexW2055408817

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.