Evidence map›Paper›PMID 31353826›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2020

Increased Adhesive Potential of Antiphospholipid Syndrome Neutrophils Mediated by β2 Integrin Mac-1.

Gautam Sule, William J Kelley, Kelsey Gockman, Srilakshmi Yalavarthi, Andrew P Vreede, Alison L Banka, Paula L Bockenstedt, Omolola Eniola-Adefeso, Jason S Knight

Open access · bronzeAbstract read
In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

37 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
  2. Article
  3. Understanding the structure of βBlood vessels, thrombosis & hemostasis · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. NETs: a new target for autoimmune disease.Frontiers in immunology · 2025
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Targeting Neutrophil βBiomolecules · 2023
    Review
  17. Review
  18. Review
  19. Article
  20. An Update on Antiphospholipid Syndrome.Current rheumatology reports · 2022
    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

9 authors at 1 institution in 1 country.

Gautam SuleUniversity of Michigan, Ann Arbor.
William J KelleyUniversity of Michigan, Ann Arbor.
Kelsey GockmanUniversity of Michigan, Ann Arbor.
Srilakshmi YalavarthiUniversity of Michigan, Ann Arbor.
Andrew P VreedeUniversity of Michigan, Ann Arbor.
Alison L BankaUniversity of Michigan, Ann Arbor.
Paula L BockenstedtUniversity of Michigan, Ann Arbor.
Omolola Eniola-AdefesoUniversity of Michigan, Ann Arbor.
Jason S KnightUniversity of Michigan, Ann Arbor.ORCID 0000-0003-0995-9771
University of Michigan · US

Funding

Michigan Institute for Clinical and Health Research (MCHR)UL1TR000433 · NCATS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MASHOUR, GEORGE ALEXANDER · 2012 to 2016
$49.9M
Purinergic modulation of the autoimmune vascular phenotypeR01HL134846 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Jason Knight · 2018 to 2026
$4.8M
Cellular Biotechnology Training Program (CBTP) - Years 31-35T32GM145304 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Guizhi Zhu · 2022 to 2026
$2.6M
Role of carrier plasma protein corona in their vascular wall localizationR01HL115138 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ENIOLA-ADEFESO, OMOLOLA · 2012 to 2016
$1.9M
Innate Immunity in the Pathogenesis of Lupus and Antiphospholipid VasculopathyK08AR066569 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KNIGHT, JASON · 2014 to 2018
$692k
NCATS NIH HHS UL1 TR000433NHLBI NIH HHS R01 HL115138NHLBI NIH HHS R01 HL134846NIAMS NIH HHS K08 AR066569NIGMS NIH HHS T32 GM145304
6 · The paper itself

Abstract

objectiveWhile the role of antiphospholipid antibodies in activating endothelial cells has been extensively studied, the impact of these antibodies on the adhesive potential of leukocytes has received less attention. This study was undertaken to investigate the extent to which antiphospholipid syndrome (APS) neutrophils adhere to resting endothelial cells under physiologic flow conditions and the surface molecules required for that adhesion.

methodsPatients with primary APS (n = 43), patients with a history of venous thrombosis but negative test results for antiphospholipid antibodies (n = 11), and healthy controls (n = 38) were studied. Cells were introduced into a flow chamber and perfused across resting human umbilical vein endothelial cells (HUVECs). Surface adhesion molecules were quantified by flow cytometry. Neutrophil extracellular trap release (NETosis) was assessed in neutrophil-HUVEC cocultures.

resultsUpon perfusion of anticoagulated blood through the flow chamber, APS neutrophils demonstrated increased adhesion as compared to control neutrophils under conditions representative of either venous (n = 8; P < 0.05) or arterial (n = 15; P < 0.0001) flow. At the same time, APS neutrophils were characterized by up-regulation of CD64, CEACAM1, β

conclusionAPS neutrophils demonstrate increased adhesive potential, which is dependent upon the activated form of Mac-1. In patients, this could lower the threshold for neutrophil-endothelium interactions, NETosis, and possibly thrombotic events.

Indexed as

Cell AdhesionAdultAgedAntiphospholipid SyndromeCase-Control StudiesEndothelial CellsExtracellular TrapsFemaleHumansHuman Umbilical Vein Endothelial CellsMacrophage-1 AntigenMaleMiddle AgedNeutrophilsYoung AdultMacrophage-1 Antigen

Identifiers

PMID31353826
PMCPMC6935403
OpenAlexW2965019847

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.