Evidence map›Paper›PMID 21187437›Full record

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

Pyk2 is required for neutrophil degranulation and host defense responses to bacterial infection.

Lynn A Kamen, Joseph Schlessinger, Clifford A Lowell

Expression of concernOpen 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. It carries an expression of concern. Cited by 36 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 2 pooled it
1.4field-weighted citation impact, top 20% 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

36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 61 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Pathogens (Basel, Switzerland) · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Frontiers in immunology · 2020
    Review
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  17. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Lynn A KamenProgram in Immunology, Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA 94143, USA.
Joseph Schlessinger
Clifford A Lowell
University of California, San Francisco · USYale University · US

Funding

Mechanisms of Neutrophil ActivationR01AI065495 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOWELL, CLIFFORD A · 2005 to 2017
$3.7M
Signaling by Cytoplasmic Tyrosine Kinases in LeukocytesR01AI068150 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOWELL, CLIFFORD A · 2006 to 2016
$3.4M
NIAID NIH HHS AI65495NIAID NIH HHS AI68150NIAID NIH HHS R01 AI065495NIAID NIH HHS R01 AI068150
6 · The paper itself

Abstract

The appropriate regulation of neutrophil activation is critical for maintaining host defense and limiting inflammation. Polymorphonuclear neutrophils (PMNs) express a number of cytoplasmic tyrosine kinases that regulate signaling pathways leading to activation. One of the most highly expressed, but least studied, kinases in PMNs is proline rich kinase 2 (Pyk2). By analogy to the related focal adhesion kinase, Pyk2 has been implicated in regulating PMN adhesion and migration; however, its physiologic function has yet to be described. Using pyk2(-/-) mice, we found that this kinase was required for integrin-mediated degranulation responses, but was not involved in adhesion-induced cell spreading or activation of superoxide production. Pyk2-deficient PMNs also manifested reduced migration on fibrinogen-coated surfaces. The absence of Pyk2 resulted in a severe reduction in paxillin and Vav phosphorylation following integrin ligation, which likely accounts for the poor degranulation and cell migration. Pyk2(-/-) mice were unable to efficiently clear infection with Staphylococcus aureus in a skin abscess model, owing in part to the poor release of granule contents at the site of infection. However, Pyk2-deficient PMNs responded normally to soluble agonists, demonstrating that this kinase functions mainly in the integrin pathway. These data demonstrate the unrealized physiologic role of this kinase in regulating the adhesion-mediated release of PMN granule contents.

Indexed as

AbscessAnimalsBone Marrow CellsCell DegranulationCell MovementDisease Models, AnimalFocal Adhesion Kinase 2Immunity, InnateIntegrinsMacrophagesMiceMice, Inbred C57BLMice, KnockoutNeutrophil ActivationNeutrophilsSignal TransductionFocal Adhesion Kinase 2IntegrinsPtk2b protein, mouse

Identifiers

PMID21187437
PMCPMC3248398
OpenAlexW1588182508

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.