Evidence map›Paper›PMID 21822296›Full record

ReviewCellular & molecular immunology2011

MicroRNA in TLR signaling and endotoxin tolerance.

Md A Nahid, Minoru Satoh, Edward Kl Chan

Open access · greenAbstract readReview
In one paragraph

Review in Cellular & molecular immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 175 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
175citing papers in PubMed, 4 pooled it
9.3field-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

175 citing papers in PubMed, 4 syntheses or guidelines pooled it, 291 citations in OpenAlex.

  1. Pooled it
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  3. Pooled it
  4. Effects of common polymorphisms rs2910164 in miR-146a and rs11614913 in miR-196a2 on susceptibility to colorectal cancer: a systematic review meta-analysis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2014
    Pooled it
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  19. Radiation-Detoxified Form of Endotoxin Effectively Activates ThInternational journal of molecular sciences · 2024
    Article
  20. Non-coding RNAs and neuroinflammation: implications for neurological disorders.Experimental biology and medicine (Maywood, N.J.) · 2024
    Review

115 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

3 authors at 1 institution in 1 country.

Md A NahidDepartment of Oral Biology, University of Florida, Gainesville, FL, USA.
Minoru Satoh
Edward Kl Chan
University of Florida · US

Funding

Novel Proteins Associated with SS-A/Ro in Target OrgansR01AI047859 · NIAID · UNIVERSITY OF FLORIDA · PI CHAN, EDWARD K · 2001 to 2011
$3.1M
IMMUNOLOGIC/GENETIC MECHANISMS IN RHEUMATIC DISEASEST32AR007603 · NIAMS · UNIVERSITY OF FLORIDA · PI REEVES, WESTLEY H · 1998 to 2014
$2.2M
NOVEL PROTEINS ASSOCIATED WITH SS-A/RO IN TARGET ORGANSR21AI047859 · NIAID · SCRIPPS RESEARCH INSTITUTE · PI CHAN, EDWARD K · 2000 to 2000
$310k
NIAID NIH HHS AI47859NIAID NIH HHS R01 AI047859NIAID NIH HHS R21 AI047859NIAMS NIH HHS T32 AR007603
6 · The paper itself

Abstract

Toll-like receptors (TLRs) in innate immune cells are the prime cellular sensors for microbial components. TLR activation leads to the production of proinflammatory mediators and thus TLR signaling must be properly regulated by various mechanisms to maintain homeostasis. TLR4-ligand lipopolysaccharide (LPS)-induced tolerance or cross-tolerance is one such mechanism, and it plays an important role in innate immunity. Tolerance is established and sustained by the activity of the microRNA miR-146a, which is known to target key elements of the myeloid differentiation factor 88 (MyD88) signaling pathway, including IL-1 receptor-associated kinase (IRAK1), IRAK2 and tumor-necrosis factor (TNF) receptor-associated factor 6 (TRAF6). In this review, we comprehensively examine the TLR signaling involved in innate immunity, with special focus on LPS-induced tolerance. The function of TLR ligand-induced microRNAs, including miR-146a, miR-155 and miR-132, in regulating inflammatory mediators, and their impact on the immune system and human diseases, are discussed. Modulation of these microRNAs may affect TLR pathway activation and help to develop therapeutics against inflammatory diseases.

Indexed as

Immunity, InnateAnimalsBacteriaBacterial InfectionsCytokinesEndotoxinsGene Expression RegulationHumansImmune System DiseasesImmune ToleranceInterleukin-1 Receptor-Associated KinasesMiceMicroRNAsMyeloid Differentiation Factor 88RatsSignal TransductionCytokinesEndotoxinsInterleukin-1 Receptor-Associated KinasesMicroRNAsMIRN132 microRNA, humanMIRN146 microRNA, humanMIRN155 microRNA, humanMyeloid Differentiation Factor 88TNF Receptor-Associated Factor 6Toll-Like Receptor 4

Identifiers

PMID21822296
PMCPMC3618661
OpenAlexW2071804009

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.