Evidence map›Paper›PMID 34031144›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2021

TRAM-Related TLR4 Pathway Antagonized by IRAK-M Mediates the Expression of Adhesion/Coactivating Molecules on Low-Grade Inflammatory Monocytes.

Kisha Pradhan, Shuo Geng, Yao Zhang, Rui-Ci Lin, Liwu Li

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Propagation of monocyte exhaustion memory and underlying mechanisms.Cell communication and signaling : CCS · 2025
    Article
  4. Clustered macrophages cooperate to eliminate tumors via coordinated intrudopodia.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Resolving neutrophils due to TRAM deletion renders protection against experimental sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  9. Imaging of atherosclerosis with [Scientific reports · 2023
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. 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

5 authors at 1 institution in 1 country.

Kisha PradhanDepartment of Biological Sciences, Virginia Polytechnic Institute and State University, Blacksburg, VA.ORCID 0000-0001-9365-3972
Shuo GengDepartment of Biological Sciences, Virginia Polytechnic Institute and State University, Blacksburg, VA.ORCID 0000-0001-9670-7294
Yao ZhangDepartment of Biological Sciences, Virginia Polytechnic Institute and State University, Blacksburg, VA.ORCID 0000-0002-0943-090X
Rui-Ci LinDepartment of Biological Sciences, Virginia Polytechnic Institute and State University, Blacksburg, VA.ORCID 0000-0002-8748-2676
Liwu LiDepartment of Biological Sciences, Virginia Polytechnic Institute and State University, Blacksburg, VA lwli@vt.edu.ORCID 0000-0001-8870-5299
Virginia Tech · US

Funding

Modulation of innate immune cellular homeostasis and inflammation resolutionR01HL115835 · NHLBI · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI LI, LIWU · 2012 to 2021
$3.6M
Altered innate leukocyte programming dynamics in sepsisR01AI136386 · NIAID · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI LI, LIWU · 2018 to 2022
$2.0M
NHLBI NIH HHS R01 HL115835NIAID NIH HHS R01 AI136386
6 · The paper itself

Abstract

Low-grade inflammatory monocytes critically contribute to the pathogenesis of chronic inflammatory diseases such as atherosclerosis. The elevated expression of coactivating molecule CD40 as well as key adhesion molecule CD11a is a critical signature of inflammatory monocytes from both human patients with coronary artery diseases as well as in animal models of atherosclerosis. In this study, we report that subclinical superlow-dose LPS, a key risk factor for low-grade inflammation and atherosclerosis, can potently trigger the induction of CD40 and CD11a on low-grade inflammatory monocytes. Subclinical endotoxin-derived monocytes demonstrate immune-enhancing effects and suppress the generation of regulatory CD8

Indexed as

AnimalsCell Adhesion MoleculesCells, CulturedInflammationInterleukin-1 Receptor-Associated KinasesMiceMice, Inbred C57BLMice, KnockoutMonocytesReceptors, InterleukinToll-Like Receptor 4Cell Adhesion MoleculesInterleukin-1 Receptor-Associated KinasesIrak3 protein, mouseReceptors, InterleukinTicam2 protein, mouseTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID34031144
PMCPMC8278277
OpenAlexW3165733509

What OpenQuestion holds

Textmetadata
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.