Evidence map›Paper›PMID 8306499›Full record

ArticleClinical and experimental immunology1994

Activated neutrophils express proteinase 3 on their plasma membrane in vitro and in vivo.

E Csernok, M Ernst, W Schmitt, D F Bainton, W L Gross

Abstract read
In one paragraph

Article in Clinical and experimental immunology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

86 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Mechanisms of vascular damage in ANCA vasculitis.Seminars in immunopathology · 2022
    Review
  8. Review
  9. Article
  10. Granulomatous Inflammation in ANCA-Associated Vasculitis.International journal of molecular sciences · 2021
    Review
  11. Article
  12. Review
  13. Article
  14. Immunopathogenesis of ANCA-Associated Vasculitis.International journal of molecular sciences · 2020
    Review
  15. Review
  16. Autoantibody Biomarkers in Rheumatic Diseases.International journal of molecular sciences · 2020
    Review
  17. Article
  18. Role of Neutrophils in Systemic Vasculitides.Frontiers in immunology · 2020
    Review
  19. Review
  20. Review

26 more citing papers are in PubMed but not listed here.

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.

E CsernokRhematological Department, Medical University Lübeck, Germany.
M Ernst
W Schmitt
D F Bainton
W L Gross

Funding

MATURATION AND FUNCTION OF BONE MARROW CELLSR01DK010486 · NIDDK · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI BAINTON, DOROTHY F · 1986 to 1993
–
NIDDK NIH HHS DK-10486
6 · The paper itself

Abstract

Apart from the diagnostic value of anti-neutrophil cytoplasmic antibodies (ANCA), their detailed characterization and that of their corresponding antigens have opened new ways for the exploration of the pathogenesis of primary systemic vasculitis. ANCA are now thought to play an important functional role via activation of phagocytic cells (e.g. polymorphonuclear neutrophils (PMN)). In this study we examined the mechanisms by which ANCA could gain access to proteinase 3 (PR3) in intact PMN, at two levels: ex vivo by analysing the presence of PR3 on the plasma membrane of PMN from patients with ANCA-associated vasculitis, and in vitro by stimulation of PMN using different cytokines, including recombinant tumour necrosis factor-alpha (rhTNF-alpha) and two forms of IL-8 (produced by monocytic and endothelial cells). Using immunocytochemical staining techniques (FACS and immunoelectronmicroscopy) PR3 has been detected on the plasma membrane of PMN from patients with active ANCA-associated vasculitis. However, this phenomenon is also seen in patients with sepsis who do not have ANCA. In addition, TNF-alpha and both forms of IL-8 act synergistically and induce a translocation of PR3 from the intragranular loci to the cell surface of PMN. These results provide strong evidence for the hypothesis that ANCA are directly pathogenic by binding to PR3 which is expressed on the cell surface of primed/activated PMN.

Indexed as

Antibodies, Antineutrophil CytoplasmicAntigens, CDAutoantibodiesCell MembraneGranulomatosis with PolyangiitisHumansInterleukin-8MyeloblastinNeutrophilsPlatelet Membrane GlycoproteinsSerine EndopeptidasesTetradecanoylphorbol AcetateTetraspanin 30Tumor Necrosis Factor-alphaAntibodies, Antineutrophil CytoplasmicAntigens, CDAutoantibodiesCD63 protein, humanInterleukin-8MyeloblastinPlatelet Membrane GlycoproteinsSerine EndopeptidasesTetradecanoylphorbol AcetateTetraspanin 30Tumor Necrosis Factor-alpha

Identifiers

PMID8306499
PMCPMC1534918

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.