Evidence map›Paper›PMID 24777746›Full record

ReviewSeminars in immunopathology2014

B cell-mediated pathogenesis of ANCA-mediated vasculitis.

J Charles Jennette, Ronald J Falk

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in immunopathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
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  12. Article
  13. Review
  14. Article
  15. B Lineage Cells in ANCA-Associated Vasculitis.International journal of molecular sciences · 2021
    Review
  16. Article
  17. Article
  18. Immunopathogenesis of ANCA-Associated Vasculitis.International journal of molecular sciences · 2020
    Review
  19. Review
  20. 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

2 authors at 1 institution in 1 country.

J Charles JennetteDepartment of Pathology and Laboratory Medicine, and Department of Medicine, School of Medicine, University of North Carolina at Chapel Hill, 308 Brinkhous-Bullitt Building, CB#7525, Chapel Hill, NC, 27599-7525, USA, jcj@med.unc.edu.
Ronald J Falk
University of North Carolina at Chapel Hill · US

Funding

Translation of Knowledge on the Pathogenesis of ANCA Disease into NovelP01DK058335 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI JENNETTE, CHARLES · 2000 to 2019
$25.9M
NIDDK NIH HHS P01 DK058335NIDDK NIH HHS P01-DK058335
6 · The paper itself

Abstract

B cells and their progeny that produce and release anti-neutrophil cytoplasmic autoantibodies (ANCA) are the primary cause for an aggressive form of necrotizing small vessel vasculitis. Cytoplasmic ANCA antigens are released at the surface and in the microenvironment of cytokine-primed neutrophils. Binding of ANCA to ANCA antigens activates neutrophils by both Fc receptor engagement and direct Fab'2 binding to antigen on the cell surface. ANCA-activated neutrophils release factors that induce alternative complement pathway activation, which establishes a potent inflammatory amplification loop that causes severe necrotizing vascular inflammation. The origin of the ANCA autoimmune response is unknown but appears to involve genetically determined HLA specificities that allow the autoimmune response to develop. One putative immunogenic mechanism begins with an immune response to a peptide that is complementary to the autoantigen and evolves through an anti-idiotypic network to produce autoantibodies to the autoantigen. Another putative immunogenic mechanism begins with an immune response to a microbe-derived molecular mimic of the autoantigen resulting in antibodies that cross-react with the autoantigen. Release of neutrophil extracellular traps, apoptosis, and increased granule protein expression of ANCA antigens may facilitate the initiation of an ANCA autoimmune response, augment established pathogenic ANCA production, or both. The ANCA B cell autoimmune response is facilitated by quantitatively and qualitatively impaired T cell and B cell suppression and by release from activated neutrophils of B cell-activating factors that enhance B cell proliferation and retard B cell apoptosis.

Indexed as

AnimalsAntibodies, Antineutrophil CytoplasmicAntigen PresentationAnti-Neutrophil Cytoplasmic Antibody-Associated VasculitisAutoantigensAutoimmunityB-LymphocytesHumansImmunomodulationNeutrophilsAntibodies, Antineutrophil CytoplasmicAutoantigens

Identifiers

PMID24777746
PMCPMC4084547
OpenAlexW2068002059

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.