Evidence map›Paper›PMID 29686675›Full record

ReviewFrontiers in immunology2018

Pathogenetic and Clinical Aspects of Anti-Neutrophil Cytoplasmic Autoantibody-Associated Vasculitides.

Peter Lamprecht, Anja Kerstein, Sebastian Klapa, Susanne Schinke, Christian M Karsten, Xinhua Yu, Marc Ehlers, Jörg T Epplen, Konstanze Holl-Ulrich, Thorsten Wiech and 19 more

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
–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

43 citing papers in PubMed.

  1. Article
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  7. Editorial: Autoimmune pre-disease.Frontiers in immunology · 2023
    Article
  8. Review
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  12. Review
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  14. Review
  15. Review
  16. Article
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  18. Article
  19. Granulomatous Inflammation in ANCA-Associated Vasculitis.International journal of molecular sciences · 2021
    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

29 authors.

Peter LamprechtDepartment of Rheumatology and Clinical Immunology, University of Lübeck, Lübeck, Germany.
Anja KersteinDepartment of Rheumatology and Clinical Immunology, University of Lübeck, Lübeck, Germany.
Sebastian KlapaDepartment of Rheumatology and Clinical Immunology, University of Lübeck, Lübeck, Germany.
Susanne SchinkeDepartment of Rheumatology and Clinical Immunology, University of Lübeck, Lübeck, Germany.
Christian M KarstenInstitute for Systemic Inflammation Research, University of Lübeck, Lübeck, Germany.
Xinhua YuXiamen-Borstel Joint Laboratory of Autoimmunity, Medical College of Xiamen University, Xiamen, China.
Marc EhlersLaboratories of Immunology and Antibody Glycan Analysis, Institute for Nutrition Medicine, University of Lübeck and University Medical Center Schleswig Holstein, Lübeck, Germany.
Jörg T EpplenDepartment of Human Genetics, Ruhr-University, Bochum, Germany.
Konstanze Holl-UlrichInstitute of Pathology, Cath. Mary's Hospital, Hamburg, Germany.
Thorsten WiechInstitute of Pathology, University Hospital Hamburg-Eppendorf, Hamburg, Germany.
Kathrin KaliesInstitute of Anatomy, University of Lübeck, Lübeck, Germany.
Tanja LangeDepartment of Rheumatology and Clinical Immunology, University of Lübeck, Lübeck, Germany.
Martin LaudienDepartment of Otorhinolaryngology, Head and Neck Surgery, University of Kiel, Kiel, Germany.
Tamas LaskayDepartment for Infectious Diseases and Microbiology, University of Lübeck, Lübeck, Germany.
Timo GemollDepartment of Surgery, Section for Translational Surgical Oncology and Biobanking, University of Lübeck, University Medical Center Schleswig-Holstein, Lübeck, Germany.
Udo SchumacherInstitute of Anatomy and Experimental Morphology, Center for Experimental Medicine, University Cancer Center, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Sebastian UllrichInstitute of Anatomy and Experimental Morphology, Center for Experimental Medicine, University Cancer Center, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Hauke BuschLübeck Institute of Experimental Dermatology, University of Lübeck, Lübeck, Germany.
Saleh IbrahimLübeck Institute of Experimental Dermatology, University of Lübeck, Lübeck, Germany.
Nicole FischerInstitute of Medical Microbiology, Virology and Hygiene, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Katrin HasselbacherDepartment of Otorhinolaryngology, University of Lübeck, Lübeck, Germany.
Ralph PriesDepartment of Otorhinolaryngology, University of Lübeck, Lübeck, Germany.
Frank PetersenPriority Area Asthma and Allergy, Research Center Borstel, Airway Research Center North (ARCN), German Center for Lung Research (DZL), Borstel, Germany.
Gesche WeppnerDepartment of Rheumatology and Clinical Immunology, University of Lübeck, Lübeck, Germany.
Rudolf ManzInstitute for Systemic Inflammation Research, University of Lübeck, Lübeck, Germany.
Jens Y HumrichDepartment of Rheumatology and Clinical Immunology, University of Lübeck, Lübeck, Germany.
Relana NieberdingDepartment of Rheumatology and Clinical Immunology, University of Lübeck, Lübeck, Germany.
Gabriela RiemekastenDepartment of Rheumatology and Clinical Immunology, University of Lübeck, Lübeck, Germany.
Antje MüllerDepartment of Rheumatology and Clinical Immunology, University of Lübeck, Lübeck, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anti-neutrophil cytoplasmic autoantibodies (ANCA) targeting proteinase 3 (PR3) and myeloperoxidase expressed by innate immune cells (neutrophils and monocytes) are salient diagnostic and pathogenic features of small vessel vasculitis, comprising granulomatosis with polyangiitis (GPA), microscopic polyangiitis, and eosinophilic GPA. Genetic studies suggest that ANCA-associated vasculitides (AAV) constitute separate diseases, which share common immunological and pathological features, but are otherwise heterogeneous. The successful therapeutic use of anti-CD20 antibodies emphasizes the prominent role of ANCA and possibly other autoantibodies in the pathogenesis of AAV. However, to elucidate causal effects in AAV, a better understanding of the complex interplay leading to the emergence of B lymphocytes that produce pathogenic ANCA remains a challenge. Different scenarios seem possible; e.g., the break of tolerance induced by a shift from non-pathogenic toward pathogenic autoantigen epitopes in inflamed tissue. This review gives a brief overview on current knowledge about genetic and epigenetic factors, barrier dysfunction and chronic non-resolving inflammation, necro-inflammatory auto-amplification of cellular death and inflammation, altered autoantigen presentation, alternative complement pathway activation, alterations within peripheral and inflamed tissue-residing T- and B-cell populations, ectopic lymphoid tissue neoformation, the characterization of PR3-specific T-cells, properties of ANCA, links between autoimmune disease and infection-triggered pathology, and animal models in AAV.

Indexed as

Anti-Neutrophil Cytoplasmic Antibody-Associated VasculitisAnimalsAntibodies, Antineutrophil CytoplasmicB-LymphocytesCell DeathComplement Pathway, AlternativeHumansImmunoglobulin GAntibodies, Antineutrophil CytoplasmicImmunoglobulin Ganti-neutrophil cytoplasmic autoantibodiesanti-neutrophil cytoplasmic autoantibody vasculitideseosinophilic granulomatosis with polyangiitisgranulomatosis with polyangiitismicroscopic polyangiitis

Identifiers

PMID29686675
PMCPMC5900791

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Registered trials

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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.