Evidence map›Paper›PMID 27593154›Full record

ArticleCellular immunology2016

TLR3 signaling is downregulated by a MAVS isoform in epithelial cells.

Omar Lakhdari, Christopher S McAllister, Michael Wang, Ivelina Minev, Lawrence S Prince, Lars Eckmann, Martin F Kagnoff

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. 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

7 authors at 1 institution in 1 country.

Omar LakhdariLaboratory of Mucosal Immunology, University of California San Diego, La Jolla, CA 92093, United States; Department of Medicine, University of California San Diego, La Jolla, CA 92093, United States. Electronic address: olakhdari@ucsd.edu.
Christopher S McAllisterLaboratory of Mucosal Immunology, University of California San Diego, La Jolla, CA 92093, United States; Department of Medicine, University of California San Diego, La Jolla, CA 92093, United States.
Michael WangLaboratory of Mucosal Immunology, University of California San Diego, La Jolla, CA 92093, United States; Department of Medicine, University of California San Diego, La Jolla, CA 92093, United States.
Ivelina MinevLaboratory of Mucosal Immunology, University of California San Diego, La Jolla, CA 92093, United States; Department of Medicine, University of California San Diego, La Jolla, CA 92093, United States.
Lawrence S PrinceDepartment of Pediatrics, University of California San Diego, La Jolla, CA 92093, United States.
Lars EckmannDepartment of Medicine, University of California San Diego, La Jolla, CA 92093, United States.
Martin F KagnoffLaboratory of Mucosal Immunology, University of California San Diego, La Jolla, CA 92093, United States; Department of Medicine, University of California San Diego, La Jolla, CA 92093, United States; Department of Pediatrics, University of California San Diego, La Jolla, CA 92093, United States.
University of California, San Diego · US

Funding

TL MOLECULES AND GAMMA-DELTA T CELLSP01DK035108 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KAGNOFF, MARTIN FREDERICK · 1986 to 2013
$19.2M
FGF-10 Expression in a Fetal Mouse Lung Model of Bronchopulmonary DysplasiaR01HL086324 · NHLBI · VANDERBILT UNIVERSITY · PI PRINCE, LAWRENCE S · 2008 to 2017
$3.7M
Transcriptional Control of Lung Macrophage DevelopmentR01HL126703 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HOFFMAN, HAROLD M, PRINCE, LAWRENCE S · 2015 to 2018
$1.6M
NHLBI NIH HHS R01 HL086324NHLBI NIH HHS R01 HL126703NIDDK NIH HHS P01 DK035108
6 · The paper itself

Abstract

Innate immune responses to dsRNA result in signaling through the TLR3 pathway and/or the RIG-I/MDA-5/MAVS pathway which can activate type I IFN, proinflammatory cytokines and apoptosis. It is not clear whether MAVS could play a role in TLR3-dependent responses to extracellular dsRNA. Using a model of epithelial cells that express a functional TLR3 signaling pathway, we found that TLR3-dependent responses to extracellular dsRNA are negatively regulated by MAVS, precisely "miniMAVS", a recently described 50kDa isoform of MAVS. This regulation of TLR3 by a MAVS isoform constitutes an endogenous regulatory mechanism in epithelial cells that could help prevent a potentially damaging excessive inflammatory response.

Indexed as

Adaptor Proteins, Signal TransducingApoptosisEpithelial CellsHCT116 CellsHumansImmunity, InnateInflammation MediatorsInterferon-betaInterferon Regulatory Factor-3NF-kappa BPoly I-CProtein IsoformsRNA, Small InterferingSignal TransductionToll-Like Receptor 3Adaptor Proteins, Signal TransducingInflammation MediatorsInterferon-betaInterferon Regulatory Factor-3IRF3 protein, humanMAVS protein, humanNF-kappa BPoly I-CProtein IsoformsRNA, Small InterferingTLR3 protein, humanToll-Like Receptor 3Epithelial cellsHCT116Interferon betaIsoformMAVSminiMAVSRegulationTLR3

Identifiers

PMID27593154
PMCPMC5125873
OpenAlexW2511420699

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.