ArticlePloS one2012
Anti-proteinase 3 anti-neutrophil cytoplasm autoantibodies recapitulate systemic vasculitis in mice with a humanized immune system.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
66 citing papers in PubMed, 1 synthesis or guideline pooled it, 165 citations in OpenAlex.
- The role of plasma exchange in antineutrophil cytoplasmic antibody-associated vasculitis: a meta-analysis.Clinical rheumatology · 2021Pooled it
- Trial
- Clinical Utility of Serial Measurements of Antineutrophil Cytoplasmic Antibodies Targeting Proteinase 3 in ANCA-Associated Vasculitis.Frontiers in immunology · 2020Trial
- Trial
- Reduced CD5(+) CD24(hi) CD38(hi) and interleukin-10(+) regulatory B cells in active anti-neutrophil cytoplasmic autoantibody-associated vasculitis permit increased circulating autoantibodies.Clinical and experimental immunology · 2015Trial
- Childhood-Onset ANCA-Associated Vasculitis: From Genetic Studies to Advances in Pathogenesis, Classification and Novel Therapeutic Approaches.International journal of molecular sciences · 2024Review
- Peripheral human red blood cell development in human immune system mouse model with heme oxygenase-1 deficiency.Blood advances · 2024Article
- Relapse Predictors in Antineutrophil Cytoplasmic Antibody (ANCA)-Associated Vasculitis.Diagnostics (Basel, Switzerland) · 2024Review
- Neutrophil extracellular traps in adult diseases and neonatal bacterial infectious diseases: A review.Heliyon · 2024Review
- Animal models for anti-neutrophil cytoplasmic antibody-associated vasculitis: Are current models good enough?Animal models and experimental medicine · 2023Review
- Mitochondrial DNA: a novel indicator of active inflammation in ANCA-associated vasculitides.Rheumatology (Oxford, England) · 2023Article
- Pathogenesis of anti-neutrophil cytoplasmic antibody-associated vasculitis.Rheumatology and immunology research · 2023Review
- Protective α1-antitrypsin effects in autoimmune vasculitis are compromised by methionine oxidation.The Journal of clinical investigation · 2022Article
- Updates in ANCA-associated vasculitis.European journal of rheumatology · 2022Article
- Review
- Neutrophil Extracellular Traps in ANCA-Associated Vasculitis and Interstitial Lung Disease: A Scoping Review.Life (Basel, Switzerland) · 2022Article
- ANCA Associated Vasculitis Subtypes: Recent Insights and Future Perspectives.Journal of inflammation research · 2022Review
- Caspase-8 activation in neutrophils facilitates autoimmune kidney vasculitis through regulating CD4Frontiers in immunology · 2022Article
- Anti-Ly6G binding and trafficking mediate positive neutrophil selection to unleash the anti-tumor efficacy of radiation therapy.Oncoimmunology · 2021Article
- Different Types of ANCA Determine Different Clinical Phenotypes and Outcome in ANCA-Associated Vasculitis (AAV).Frontiers in medicine · 2021Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Evidence is lacking for direct pathogenicity of human anti-proteinase-3 (PR3) antibodies in development of systemic vasculitis and granulomatosis with polyangiitis (GPA, Wegener's granulomatosis). Progress in study of these antibodies in rodents has been hampered by lack of PR3 expression on murine neutrophils, and by different Fc-receptor affinities for IgG across species. Therefore, we tested whether human anti-PR3 antibodies can induce acute vasculitis in mice with a human immune system. Chimeric mice were generated by injecting human haematopoietic stem cells into irradiated NOD-scid-IL2Rγ⁻/⁻ mice. Matched chimera mice were treated with human IgG from patients with: anti-PR3 positive renal and lung vasculitis; patients with non-vasculitic renal disease; or healthy controls. Six-days later, 39% of anti-PR3 treated mice had haematuria, compared with none of controls. There was punctate bleeding on the surface of lungs of anti-PR3 treated animals, with histological evidence of vasculitis and haemorrhage. Anti-PR3 treated mice had mild pauci-immune proliferative glomerulonephritis, with infiltration of human and mouse leukocytes. In 3 mice (17%) more severe glomerular injury was present. There were no glomerular changes in controls. Human IgG from patients with anti-PR3 autoantibodies is therefore pathogenic. This model of anti-PR3 antibody-mediated vasculitis may be useful in dissecting mechanisms of microvascular injury.
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What OpenQuestion holds
Registered trials
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.