Evidence map›Paper›PMID 26651944›Full record

ArticleCell host & microbe2015

A Single Bacterial Immune Evasion Strategy Dismantles Both MyD88 and TRIF Signaling Pathways Downstream of TLR4.

Charles V Rosadini, Ivan Zanoni, Charlotte Odendall, Erin R Green, Michelle K Paczosa, Naomi H Philip, Igor E Brodsky, Joan Mecsas, Jonathan C Kagan

Open access · bronzeAbstract read
In one paragraph

Article in Cell host & microbe, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

33 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
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  9. Review
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  12. Role of pyroptosis in inflammation and cancer.Cellular & molecular immunology · 2022
    Review
  13. Molecular medicine reports · 2022
    Article
  14. Article
  15. Article
  16. Interferons: Tug of War Between Bacteria and Their Host.Frontiers in cellular and infection microbiology · 2021
    Review
  17. Article
  18. Article
  19. Article
  20. Review
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

9 authors at 3 institutions in 2 countries.

Charles V RosadiniHarvard Medical School and Division of Gastroenterology, Boston Children's Hospital, Boston, MA 02115, USA.
Ivan ZanoniHarvard Medical School and Division of Gastroenterology, Boston Children's Hospital, Boston, MA 02115, USA; Department of Biotechnology and Biosciences, University of Milano-Bicocca, Milan 20126, Italy; Unit of Cell Signalling and Innate Immunity, Humanitas Clinical and Research Center, Rozzano 20089, Italy.
Charlotte OdendallHarvard Medical School and Division of Gastroenterology, Boston Children's Hospital, Boston, MA 02115, USA.
Erin R GreenGraduate Program in Molecular Microbiology, Sackler School of Biomedical Sciences, Tufts University School of Medicine, Boston, MA 02111, USA.
Michelle K PaczosaGraduate Program in Immunology, Sackler School of Biomedical Sciences, Tufts University School of Medicine, Boston, MA 02111, USA.
Naomi H PhilipDepartment of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Igor E BrodskyDepartment of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Joan MecsasGraduate Program in Molecular Microbiology, Sackler School of Biomedical Sciences, Tufts University School of Medicine, Boston, MA 02111, USA; Graduate Program in Immunology, Sackler School of Biomedical Sciences, Tufts University School of Medicine, Boston, MA 02111, USA.
Jonathan C KaganHarvard Medical School and Division of Gastroenterology, Boston Children's Hospital, Boston, MA 02115, USA. Electronic address: jonathan.kagan@childrens.harvard.edu.
Boston Children's Hospital · USTufts University · USUniversity of Pennsylvania · US

Funding

STRUCTURE-FUNCTION RELATIONSHIPS IN THE ALIMENTARY TRACTP30DK034854 · NIDDK · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WAYNE I LENCER · 1986 to 2026
$32.4M
Initiation and Regulation of Antiviral Innate ImmunityR01AI093589 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI KAGAN, JONATHAN C · 2011 to 2020
$4.4M
Initiation and regulation of antibacterial innate immunityR01AI113166 · NIAID · TUFTS UNIVERSITY BOSTON · PI MECSAS, JOAN C · 2014 to 2018
$2.4M
Modulation of Inflammasome Activation by YersiniaR01AI103062 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI BRODSKY, IGOR E · 2013 to 2016
$1.7M
Initiation and Regulation of Antiviral Innate ImmunityR56AI093589 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI KAGAN, JONATHAN C · 2021 to 2021
$531k
Cellular and molecular aspects of Toll-like receptor signal transduction.R00AI072955 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI KAGAN, JONATHAN C · 2008 to 2009
$498k
Initiation and regulation of antibacterial innate immunityR56AI113141 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI KAGAN, JONATHAN C · 2014 to 2014
$456k
Defining non-transcriptional innate immune responses to bacterial endotoxinR56AI103082 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI KAGAN, JONATHAN C · 2013 to 2013
$411k
Regulation of Innate Immunity in Intestinal Epithelial CellsF32DK102317 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI ROSADINI, CHARLES VICTOR · 2014 to 2015
$109k
Cellular and molecular aspects of Toll-like receptor signal transduction.K99AI072955 · NIAID · YALE UNIVERSITY · PI KAGAN, JONATHAN C · 2007 to 2007
$90k
NIAID NIH HHS AI113141NIAID NIH HHS AI113166NIAID NIH HHS K99 AI072955NIAID NIH HHS R00 AI072955NIAID NIH HHS R01 AI093589NIAID NIH HHS R01 AI103062NIAID NIH HHS R01 AI113166NIAID NIH HHS R56 AI093589NIAID NIH HHS R56 AI103082NIAID NIH HHS R56 AI113141NIDDK NIH HHS DK102317-01NIDDK NIH HHS F32 DK102317NIDDK NIH HHS P30 DK034854NIDDK NIH HHS P30 DK34854
6 · The paper itself

Abstract

During bacterial infections, Toll-like receptor 4 (TLR4) signals through the MyD88- and TRIF-dependent pathways to promote pro-inflammatory and interferon (IFN) responses, respectively. Bacteria can inhibit the MyD88 pathway, but if the TRIF pathway is also targeted is unclear. We demonstrate that, in addition to MyD88, Yersinia pseudotuberculosis inhibits TRIF signaling through the type III secretion system effector YopJ. Suppression of TRIF signaling occurs during dendritic cell (DC) and macrophage infection and prevents expression of type I IFN and pro-inflammatory cytokines. YopJ-mediated inhibition of TRIF prevents DCs from inducing natural killer (NK) cell production of antibacterial IFNγ. During infection of DCs, YopJ potently inhibits MAPK pathways but does not prevent activation of IKK- or TBK1-dependent pathways. This singular YopJ activity efficiently inhibits TLR4 transcription-inducing activities, thus illustrating a simple means by which pathogens impede innate immunity.

Indexed as

Host-Pathogen InteractionsImmune EvasionSignal TransductionAdaptor Proteins, Vesicular TransportAnimalsBacterial ProteinsCells, CulturedDendritic CellsMacrophagesMiceMyeloid Differentiation Factor 88Toll-Like Receptor 4Yersinia pseudotuberculosisAdaptor Proteins, Vesicular TransportBacterial ProteinsMyd88 protein, mouseMyeloid Differentiation Factor 88Ticam1 protein, mouseTlr4 protein, mouseToll-Like Receptor 4YopP protein, Yersinia

Identifiers

PMID26651944
PMCPMC4685476
OpenAlexW2194029163

What OpenQuestion holds

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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.