ReviewClinical and experimental immunology2011
Pathogenesis of anti-neutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis.
Review in Clinical and experimental immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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
21 citing papers in PubMed, 46 citations in OpenAlex.
- Mycophenolate mofetil in patients with anti-neutrophil cytoplasmic antibody-associated vasculitis: a prospective pharmacokinetics and clinical study.Clinical and experimental immunology · 2014Trial
- The emerging role of neutrophil extracellular traps in autoimmune and autoinflammatory diseases.MedComm · 2025Review
- Propylthiouracil-induced vasculitis with alveolar hemorrhage after 31 years of treatment: a case report.Clinical diabetes and endocrinology · 2024Article
- Exploring Frequencies of Circulating Specific Th17 Cells against Myeloperoxidase and Proteinase 3 in ANCA Associated Vasculitis.International journal of molecular sciences · 2019Article
- Molecular mechanisms regulating immune responses in thromboangiitis obliterans: A comprehensive review.Iranian journal of basic medical sciences · 2019Review
- Neutrophil Heterogeneity as Therapeutic Opportunity in Immune-Mediated Disease.Frontiers in immunology · 2019Review
- Proteinase 3; a potential target in chronic obstructive pulmonary disease and other chronic inflammatory diseases.Respiratory research · 2018Review
- Pathogenesis and treatment of ANCA-associated vasculitis-a role for complement.Pediatric nephrology (Berlin, Germany) · 2018Review
- Possible intrinsic association of anti-neutrophil cytoplasmic antibody-associated vasculitis coexisting with multiple myeloma.Oncology letters · 2016Article
- Complement-mediated 'bystander' damage initiates host NLRP3 inflammasome activation.Journal of cell science · 2016Article
- High-mobility group box 1 potentiates antineutrophil cytoplasmic antibody-inducing neutrophil extracellular traps formation.Arthritis research & therapy · 2016Article
- Vasculitis: do we know more to classify better?Pediatric nephrology (Berlin, Germany) · 2015Review
- The role of necrotic cell death in the pathogenesis of immune mediated nephropathies.Clinical immunology (Orlando, Fla.) · 2014Review
- Eosinophils in vasculitis: characteristics and roles in pathogenesis.Nature reviews. Rheumatology · 2014Review
- Overlap between dermatomyositis and ANCA vasculitides.Clinical kidney journal · 2014Article
- Intravascular immunity as a key to systemic vasculitis: a work in progress, gaining momentum.Clinical and experimental immunology · 2014Review
- Relation between asymptomatic proteinase 3 antibodies and future granulomatosis with polyangiitis.Clinical journal of the American Society of Nephrology : CJASN · 2013Article
- Broadening the translational immunology landscape.Clinical and experimental immunology · 2012Article
- Genetically distinct subsets within ANCA-associated vasculitis.The New England journal of medicine · 2012Article
- Association Between Serum Alarmin Levels and Disease-specific Indices in Patients With Anti-neutrophil Cytoplasmic Antibody-associated Vasculitis.In vivo (Athens, Greece)Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anti-neutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis is an autoimmune disease in which the contributions of genetic, epigenetic and environmental factors to aetiology and pathogenesis are being unravelled. The ANCA immunoglobulin G targeting proteinase 3 and myeloperoxidase affects several neutrophil functions, usually to augment or dysregulate these, promoting a proinflammatory phenotype whereby neutrophils have enhanced capabilities of causing collateral damage to endothelial and other cells. In addition, B cells are intimately involved in pathogenesis as anti-B cell therapies are highly effective, but the manner of this involvement still needs to be delineated. Similarly, the T cell compartment is disturbed in ANCA vasculitis and numerous alterations in T cell subsets have been described, but recognition of a novel CD8(+) T cell transcription signature which can predict likelihood of relapse in ANCA vasculitis indicates that more needs to be learnt about the influence of T cells in the disease process. Finally, the role of the alternative complement pathway and the potential therapeutic value of its neutralization is under active investigation after compelling studies in murine models have demonstrated that C5 and factor-B knock-out mice are protected.
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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.