Evidence map›Paper›PMID 21804015›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

TLT2 potentiates neutrophil antibacterial activity and chemotaxis in response to G protein-coupled receptor-mediated signaling.

Matthew M Halpert, Kimberly A Thomas, R Glenn King, Louis B Justement

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. B7-H3 in Brain Malignancies: Immunology and Immunotherapy.International journal of biological sciences · 2023
    Review
  5. International journal of molecular sciences · 2022
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Multiple Phenotypic Changes Define Neutrophil Priming.Frontiers in cellular and infection microbiology · 2017
    Review
  12. Article
  13. Immunoreceptors on neutrophils.Seminars in immunology · 2016
    Review
  14. Article
  15. 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

4 authors at 1 institution in 1 country.

Matthew M HalpertDepartment of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Kimberly A Thomas
R Glenn King
Louis B Justement
University of Alabama at Birmingham · US

Funding

IMMUNOLOGIC DISEASES AND BASIC IMMUNOLOGYT32AI007051 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Laurie Ellen Harrington · 1985 to 2026
$13.1M
Howard Hughes Medical Institute 56005705NIAID NIH HHS T32 AI007051NIAID NIH HHS T32 AI 007051-33
6 · The paper itself

Abstract

Receptors encoded within the Trem locus have been shown to play an important role in modulating the cellular response to pattern recognition receptor signaling. TREM-like transcript 2 (TLT2) is a member of the Trem locus that is conserved in mouse and human. TLT2 exhibits a unique expression pattern in that it is expressed on cells of the myeloid and lymphoid lineage, suggesting that it plays a role in both innate and adaptive immunity. In this work, studies reveal that TLT2 plays an important role in potentiating neutrophil antibacterial activity and chemotaxis. TLT2 ligation enhances the neutrophil response to the formylated peptide FMLF, leading to increased reactive oxygen species production, degranulation, and chemotaxis. Moreover, TLT2 has the ability to specifically potentiate neutrophil activation and chemotaxis in response to a range of agonists that bind to G protein-coupled receptors, as it does not potentiate the response of cells to growth factor receptor-, Fc receptor-, or TLR-mediated signaling. Finally, TLT2 ligation potentiates the recruitment of neutrophils to sites of inflammation in vivo. These findings reveal a novel functional role for TLT2 that involves potentiation of neutrophil responses to G protein-coupled receptor signaling. Thus, TLT2 appears to play an important role in enhancing the innate immune response via a novel molecular mechanism.

Indexed as

AnimalsCell SeparationChemotaxis, LeukocyteFlow CytometryImmunity, InnateInflammationMiceMice, Inbred C57BLNeutrophil ActivationNeutrophilsReceptors, G-Protein-CoupledReceptors, ImmunologicSignal TransductionReceptors, G-Protein-CoupledReceptors, ImmunologicTLT-2 protein, mouse

Identifiers

PMID21804015
PMCPMC3159717
OpenAlexW2127972108

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.