Evidence map›Paper›PMID 23685129›Full record

ArticleVascular pharmacology

Agonistic anti-ICAM-1 antibodies in scleroderma: activation of endothelial pro-inflammatory cascades.

Sabine I Wolf, Sarah Howat, David J Abraham, Jeremy D Pearson, Charlotte Lawson

Open access · hybridAbstract read
In one paragraph

Article in Vascular pharmacology. 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
1.9field-weighted citation impact, top 15% 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, 43 citations in OpenAlex.

  1. Review
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  11. Autoantibody Biomarkers in Rheumatic Diseases.International journal of molecular sciences · 2020
    Review
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  15. Review
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  17. Functional autoantibodies in systemic sclerosis.Seminars in immunopathology · 2015
    Review
  18. Review
  19. 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 3 institutions in 1 country.

Sabine I WolfDepartment of Comparative Biomedical Sciences, The Royal Veterinary College, London, UK.
Sarah Howat
David J Abraham
Jeremy D Pearson
Charlotte Lawson
King's College London · GBRoyal Veterinary College · GBThe Royal Free Hospital · GB

Funding

Arthritis Research UK 19427British Heart Foundation PG/05/114
6 · The paper itself

Abstract

backgroundScleroderma (SSc) is a complex autoimmune disorder that can be characterised by the presence 2of circulating autoantibodies to nuclear, cytoplasmic and cell surface antigens. In particular antibodies directed against endothelial cell antigens (anti-endothelial cell antibodies; AECA) have been detected. ICAM-1 is an adhesion molecule expressed on the surface of human endothelial cells. We have previously shown that cross-linking ICAM-1 with monoclonal antibodies leads to pro-inflammatory activation of human endothelial and vascular smooth muscle cells and that cardiac transplant recipients with transplant associated vasculopathy make antibodies directed against ICAM-1.

objectivesTo determine whether SSc patients make antibodies directed against ICAM-1 and whether these antibodies induce pro-inflammatory activation of human endothelial cells in vitro.

methodsUsing recombinant ICAM-1 as capture antigen, an ELISA was developed to measure ICAM-1 antibodies in sera from SSc patients. Antibodies were purified using ICAM-1 micro-affinity columns. HUVEC were incubated with purified anti-ICAM-1 antibodies and generation of reactive oxygen species, and expression of VCAM-1 was measured.

resultsSignificantly elevated levels of anti-ICAM-1 antibodies were detected in patients with diffuse (dSSc; 10/31 32%) or limited (lSSc; 14/36 39%) scleroderma. Cross-linking of HUVEC with purified anti-ICAM-1 antibodies caused a significant increase in ROS production (2.471±0.408 fold increase above untreated after 150 min p<0.001), and significant increase in VCAM-1 expression (10.6±1.77% vs 4.12±1.33%, p<0.01).

conclusionAECA from SSc patients target specific endothelial antigens including ICAM-1, and cause pro-inflammatory activation of human endothelial cells, suggesting that they are not only a marker of disease but that they contribute to its progression.

Indexed as

AntibodiesAutoantibodiesAutoimmune DiseasesCells, CulturedEndothelial CellsEndothelium, VascularHumansHuman Umbilical Vein Endothelial CellsInflammationIntercellular Adhesion Molecule-1Reactive Oxygen SpeciesScleroderma, DiffuseScleroderma, LimitedVascular Cell Adhesion Molecule-1Antibodiesanti-endothelial cell antibodyAutoantibodiesIntercellular Adhesion Molecule-1Reactive Oxygen SpeciesVascular Cell Adhesion Molecule-1AutoantibodiesICAM-1Systemic sclerosisVascular inflammation

Identifiers

PMID23685129
PMCPMC3731553
OpenAlexW1983982569

What OpenQuestion holds

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LicenceCC BY
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.