Evidence map›Paper›PMID 22266279›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Proteinase 3 contributes to transendothelial migration of NB1-positive neutrophils.

Christopher J Kuckleburg, Sarah B Tilkens, Sentot Santoso, Peter J Newman

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

41 citing papers in PubMed, 77 citations in OpenAlex.

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  7. TheInternational journal of molecular sciences · 2024
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  20. Endogenous stimulation is responsible for the high frequency of IL-17A-producing neutrophils in patients with rheumatoid arthritis.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2019
    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 2 institutions in 2 countries.

Christopher J KuckleburgBlood Research Institute, Blood Center of Wisconsin, Milwaukee, WI 53201, USA. Christopher.Kuckleburg@bcw.edu
Sarah B Tilkens
Sentot Santoso
Peter J Newman
Versiti Blood Center of Wisconsin · USUniversity of Giessen · DE

Funding

MOLECULAR BIOLOGY &FUNCTION OF PLATELET MEMBRANE GP130R01HL040926 · NHLBI · VERSITI WISCONSIN, INC. · PI NEWMAN, PETER J · 1988 to 2017
$7.4M
RESEARCH TRAINING IN TRANSFUSION SCIENCET32HL007209 · NHLBI · VERSITI WISCONSIN, INC. · PI WHITE, II, GILBERT C. · 1985 to 2019
$2.9M
NHLBI NIH HHS R01 HL040926NHLBI NIH HHS T32 HL007209
6 · The paper itself

Abstract

Neutrophil transmigration requires the localization of neutrophils to endothelial cell junctions, in which receptor-ligand interactions and the action of serine proteases promote leukocyte diapedesis. NB1 (CD177) is a neutrophil-expressed surface molecule that has been reported to bind proteinase 3 (PR3), a serine protease released from activated neutrophils. PR3 has demonstrated proteolytic activity on a number of substrates, including extracellular matrix proteins, although its role in neutrophil transmigration is unknown. Recently, NB1 has been shown to be a heterophilic binding partner for the endothelial cell junctional protein, PECAM-1. Disrupting the interaction between NB1 and PECAM-1 significantly inhibits neutrophil transendothelial cell migration on endothelial cell monolayers. Because NB1 interacts with endothelial cell PECAM-1 at cell junctions where transmigration occurs, we considered that NB1-PR3 interactions may play a role in aiding neutrophil diapedesis. Blocking Abs targeting the heterophilic binding domain of PECAM-1 significantly inhibited transmigration of NB1-positive neutrophils through IL-1β-stimulated endothelial cell monolayers. PR3 expression and activity were significantly increased on NB1-positive neutrophils following transmigration, whereas neutrophils lacking NB1 demonstrated no increase in PR3. Finally, using selective serine protease inhibitors, we determined that PR3 activity facilitated transmigration of NB1-positive neutrophils under both static and flow conditions. These data demonstrate that PR3 contributes in the selective recruitment of the NB1-positive neutrophil population.

Indexed as

Enzyme ActivationGene Expression RegulationGPI-Linked ProteinsHumansHuman Umbilical Vein Endothelial CellsIsoantigensMyeloblastinNeutrophilsReceptors, Cell SurfaceTransendothelial and Transepithelial MigrationCD177 protein, humanGPI-Linked ProteinsIsoantigensMyeloblastinReceptors, Cell Surface

Identifiers

PMID22266279
PMCPMC3288489
OpenAlexW2171139467

What OpenQuestion holds

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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.