Evidence map›Paper›PMID 23239500›Full record

ArticleAmerican journal of respiratory cell and molecular biology2013

Bruton's tyrosine kinase mediates FcγRIIa/Toll-like receptor-4 receptor crosstalk in human neutrophils.

Agnieszka Krupa, Rafal Fudala, Jon M Florence, Torry Tucker, Timothy C Allen, Theodore J Standiford, Rafal Luchowski, Marek Fol, Moshiur Rahman, Zygmunt Gryczynski and 2 more

Abstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.8field-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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Review
  7. Article
  8. p65BTK Is a Novel Biomarker and Therapeutic Target in Solid Tumors.Frontiers in cell and developmental biology · 2021
    Review
  9. Article
  10. Article
  11. Promoting Neutrophil Apoptosis to Treat Acute Lung Injury.American journal of respiratory and critical care medicine · 2019
    Article
  12. Review
  13. Inhibiting Bruton's tyrosine kinase rescues mice from lethal influenza-induced acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2018
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Targeting the Fc receptor in autoimmune disease.Expert opinion on therapeutic targets · 2014
    Review
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

12 authors at 5 institutions in 2 countries.

Agnieszka KrupaDepartment of Cellular and Molecular Biology, University of Texas Health Science Center at Tyler, Tyler, TX 75708, USA.
Rafal Fudala
Jon M Florence
Torry Tucker
Timothy C Allen
Theodore J Standiford
Rafal Luchowski
Marek Fol
Moshiur Rahman
Zygmunt Gryczynski
Ignacy Gryczynski
Anna K Kurdowska
The University of Texas at Tyler · USUniversity of North Texas · USInstitute for Medical Biology · PLThe University of Texas Health Science Center at Tyler · USUniversity of Michigan · US

Funding

Impact of IL-8 Bound to the Anti-IL-8 AutoantibodyR01HL073245 · NHLBI · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI KURDOWSKA, ANNA K · 2004 to 2007
$1.1M
NHLBI NIH HHS HL073245NHLBI NIH HHS R01 HL073245
6 · The paper itself

Abstract

Previous observations by our laboratory indicate that the presence of anti-IL-8 autoantibody:IL-8 immune complexes in lung fluids from patients with acute lung injury/acute respiratory distress syndrome (ALI/ARDS) comprises an important prognostic indicator in the development and ultimate outcome of ALI/ARDS. We also showed that these complexes display proinflammatory activity toward neutrophils through the engagement of FcγRIIa receptors. Because sepsis is one of the most common risk factors for ALI/ARDS, the initial goal of our present study involved investigating the effects of LPS on the expression of FcγRIIa receptors in neutrophils. Our results indicate that LPS triggers an increase in the expression of FcγRIIa on the neutrophil surface, which leads to shortening of the molecular distance between FcγRIIa and Toll-like receptor-4 (TLR4). When such neutrophils are stimulated with anti-IL-8:IL-8 complexes, the TLR4 cascade becomes activated via the engagement of FcγRIIa. The underlying molecular mechanism has been subsequently examined and involves Bruton's tyrosine kinase (Btk). In conclusion, our study reveals the existence of Btk-dependent molecular cooperation between FcγRIIa and TLR4 signaling cascades in LPS-"primed" human neutrophils. Furthermore, we used fluorescence lifetime imaging to study the interactions between TLR4 and FcγRIIa in human alveolar neutrophils from patients with ALI/ARDS. The results from these experiments confirm the existence of the molecular cooperation between TLR4 and FcγRIIa.

Indexed as

Receptor Cross-TalkAgammaglobulinaemia Tyrosine KinaseBlotting, WesternFluorescence Resonance Energy TransferHumansMicroscopy, ConfocalNeutrophilsProtein BindingProtein-Tyrosine KinasesReceptors, IgGSignal TransductionToll-Like Receptor 4Agammaglobulinaemia Tyrosine KinaseBTK protein, humanFc gamma receptor IIAProtein-Tyrosine KinasesReceptors, IgGToll-Like Receptor 4

Identifiers

PMID23239500
PMCPMC3604059
OpenAlexW2032874971

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.