Evidence map›Paper›PMID 20634142›Full record

ArticleClinical immunology (Orlando, Fla.)2010

TLR signaling and effector functions are intact in XLA neutrophils.

Thomas U Marron, Kaileen Rohr, Monica Martinez-Gallo, Joyce Yu, Charlotte Cunningham-Rundles

Open access · greenAbstract read
In one paragraph

Article in Clinical immunology (Orlando, Fla.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Autoimmunity in Primary Immunodeficiencies (PID).Clinical reviews in allergy & immunology · 2023
    Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Toll-like receptor signaling in primary immune deficiencies.Annals of the New York Academy of Sciences · 2015
    Review
  14. Article
  15. Article
  16. Toll-like receptor function in primary B cell defects.Frontiers in bioscience (Elite edition) · 2012
    Review
  17. Article
  18. Article
  19. Article
  20. 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 2 institutions in 1 country.

Thomas U MarronImmunology Institute, Mount Sinai School of Medicine, New York, NY, USA.
Kaileen Rohr
Monica Martinez-Gallo
Joyce Yu
Charlotte Cunningham-Rundles
Icahn School of Medicine at Mount Sinai · USCornell University · US

Funding

Regulation of IgA class switching in the intestinal mucosaP01AI061093 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI CUNNINGHAM-RUNDLES, CHARLOTTE · 2004 to 2021
$29.8M
TARGETING PRIMARY IMMUNODEFICIENCY AMONG MINORITIESR18AI048693 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI CUNNINGHAM-RUNDLES, CHARLOTTE · 2000 to 2016
$6.2M
Exposporium determinants of Bacillus anthracisR21AI101093 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI STEWART, GEORGE C. · 2012 to 2013
$390k
NIAID NIH HHS AI 101093NIAID NIH HHS AI-467320NIAID NIH HHS AI-48693NIAID NIH HHS P01 AI061093NIAID NIH HHS R18 AI048693NIAID NIH HHS R21 AI101093
6 · The paper itself

Abstract

Toll-like receptors (TLRs) are essential components of the innate immune system, and their ligands are important activators of neutrophils. Bruton's tyrosine kinase (Btk) has been reported to mediate signaling through toll-like receptors (TLRs) in many cell types, however, the role of Btk in TLR activation of neutrophils remains unclear. Impaired TLR-induced neutrophil function was found in mice with loss of Btk and in humans with TLR-signaling defects, but the integrity of TLR pathways in X-linked agammaglobulinemia (XLA) neutrophils has not been assessed. In this study LPS (TLR4) or an imidazoquinoline compound (TLR7/8) activated XLA neutrophil shedding of surface CD62L, and phosphorylated MAP kinases p38, JNK and ERK. TLR activation also induced normal respiratory burst and retarded apoptosis for XLA neutrophils, comparable to normal controls. These data demonstrate that the loss of Btk in XLA neutrophils does not impair functional responses to TLR signals.

Indexed as

AdolescentAdultAgammaglobulinaemia Tyrosine KinaseAgammaglobulinemiaApoptosisChildGenetic Diseases, X-LinkedGranulocyte-Macrophage Colony-Stimulating FactorHumansImidazolesLipopolysaccharidesL-SelectinMitogen-Activated Protein KinasesNeutrophil ActivationNeutrophilsPhosphorylationAgammaglobulinaemia Tyrosine KinaseBTK protein, humanBtk protein, mouseCL097 compoundGranulocyte-Macrophage Colony-Stimulating FactorImidazolesLipopolysaccharidesL-SelectinMitogen-Activated Protein KinasesProtein-Tyrosine KinasesQuinolinesReactive Oxygen SpeciesTetradecanoylphorbol AcetateToll-Like Receptors

Identifiers

PMID20634142
PMCPMC2941555
OpenAlexW2080949615

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.