Evidence map›Paper›PMID 34204207›Full record

ReviewInternational journal of molecular sciences2021

Granulomatous Inflammation in ANCA-Associated Vasculitis.

Antje Müller, Bettina Krause, Anja Kerstein-Stähle, Sara Comdühr, Sebastian Klapa, Sebastian Ullrich, Konstanze Holl-Ulrich, Peter Lamprecht

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 2 pooled it
5.0field-weighted citation impact, top 4% 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

17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. The theory of the inflammatory ecosystem.Science China. Life sciences · 2026
    Review
  4. Article
  5. Article
  6. Assessment of cardiovascular risk in patients with ANCA-associated vasculitis: A systematic review and meta-analysis.International journal of cardiology. Cardiovascular risk and prevention · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
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  15. Review
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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

8 authors at 4 institutions in 1 country.

Antje MüllerDepartment of Rheumatology & Clinical Immunology, University of Luebeck, 23562 Luebeck, Germany.
Bettina KrauseDepartment of Rheumatology & Clinical Immunology, University of Luebeck, 23562 Luebeck, Germany.
Anja Kerstein-StähleDepartment of Rheumatology & Clinical Immunology, University of Luebeck, 23562 Luebeck, Germany.ORCID 0000-0003-1841-7974
Sara ComdührDepartment of Rheumatology & Clinical Immunology, University of Luebeck, 23562 Luebeck, Germany.
Sebastian KlapaDepartment of Rheumatology & Clinical Immunology, University of Luebeck, 23562 Luebeck, Germany.ORCID 0000-0002-0012-0163
Sebastian UllrichInstitute of Anatomy & Experimental Morphology, University Hospital Hamburg-Eppendorf, University of Hamburg, 20251 Hamburg, Germany.
Konstanze Holl-UlrichPathologie Hamburg, Labor Lademannbogen MVZ GmbH, 22339 Hamburg, Germany.
Peter LamprechtDepartment of Rheumatology & Clinical Immunology, University of Luebeck, 23562 Luebeck, Germany.
University of Lübeck · DEUniversität Hamburg · DEChristian-Albrechts-Universität zu Kiel · DEPathologie Hamburg-West · DE

Funding

Bundesministerium für Bildung, Wissenschaft und Forschung 01EC1901D
6 · The paper itself

Abstract

ANCA-associated vasculitis (AAV) comprises granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA), and eosinophilic granulomatosis with polyangiitis (EGPA). While systemic vasculitis is a hallmark of all AAV, GPA is characterized by extravascular granulomatous inflammation, preferentially affecting the respiratory tract. The mechanisms underlying the emergence of neutrophilic microabscesses; the appearance of multinucleated giant cells; and subsequent granuloma formation, finally leading to scarred or destroyed tissue in GPA, are still incompletely understood. This review summarizes findings describing the presence and function of molecules and cells contributing to granulomatous inflammation in the respiratory tract and to renal inflammation observed in GPA. In addition, factors affecting or promoting the development of granulomatous inflammation such as microbial infections, the nasal microbiome, and the release of damage-associated molecular patterns (DAMP) are discussed. Further, on the basis of numerous results, we argue that, in situ, various ways of exposure linked with a high number of infiltrating proteinase 3 (PR3)- and myeloperoxidase (MPO)-expressing leukocytes lower the threshold for the presentation of an altered PR3 and possibly also of MPO, provoking the local development of ANCA autoimmune responses, aided by the formation of ectopic lymphoid structures. Although extravascular granulomatous inflammation is unique to GPA, similar molecular and cellular patterns can be found in both the respiratory tract and kidney tissue of GPA and MPA patients; for example, the antimicrobial peptide LL37, CD163

Indexed as

Disease SusceptibilityAnimalsAntibodies, Antineutrophil CytoplasmicAnti-Neutrophil Cytoplasmic Antibody-Associated VasculitisAutoimmune DiseasesAutoimmunityBiomarkersCell MovementDisease ManagementGranulomatosis with PolyangiitisHumansImmunity, InnateImmunohistochemistryOrgan SpecificityAntibodies, Antineutrophil CytoplasmicBiomarkersautoimmune diseasedestructiongranulomagranulomatosis with polyangiitisinflammationtissue

Identifiers

PMID34204207
PMCPMC8234846
OpenAlexW3167563462

What OpenQuestion holds

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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.