ArticleThe American journal of pathology2007
Alternative complement pathway in the pathogenesis of disease mediated by anti-neutrophil cytoplasmic autoantibodies.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 270 papers, 3 of them syntheses that pooled it.
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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
270 citing papers in PubMed, 3 syntheses or guidelines pooled it, 557 citations in OpenAlex.
- Non-invasive biomarkers of disease activity and organ damage in ANCA-associated vasculitis: a systematic review.RMD open · 2024Pooled it
- Efficacy of plasma exchange for antineutrophil cytoplasmic antibody-associated systemic vasculitis: a systematic review and meta-analysis.Arthritis research & therapy · 2021Pooled it
- The alternative complement pathway in ANCA-associated vasculitis: further evidence and a meta-analysis.Clinical and experimental immunology · 2020Pooled it
- Circulating autoreactive proteinase 3+ B cells and tolerance checkpoints in ANCA-associated vasculitis.JCI insight · 2021Trial
- Marginal-Zone B-Cells Are Main Producers of IgM in Humans, and Are Reduced in Patients With Autoimmune Vasculitis.Frontiers in immunology · 2018Trial
- Acute renal injury in ANCA-associated glomerulonephritis: etiology related to acute tubulointerstitial injury versus glomerular injury.Renal failure · 2026Article
- Complement and kidney diseases: unlocking the opportunity of targeted treatments for glomerular diseases, including IgA nephropathy.Pediatric nephrology (Berlin, Germany) · 2026Review
- Anti-neutrophil cytoplasmic antibody-associated vasculitis: biological insights and biomarker-guided disease management.Nature reviews. Nephrology · 2026Review
- Association of FHR5 With Disease Severity in ANCA-Associated Vasculitis.Kidney international reports · 2026Article
- Article
- Renal Involvement in Pediatric Small-Vessel Vasculitis: A Comprehensive Review of Clinical Impact, Diagnosis, and Management.Medical sciences (Basel, Switzerland) · 2026Review
- The evolving landscape of complement therapeutics in rheumatology.Annals of the rheumatic diseases · 2026Review
- Characterization of Circulating Immune Complexes in Patients with Myeloperoxidase-Antineutrophil Cytoplasmic Antibody-Associated Glomerulonephritis.International journal of molecular sciences · 2026Article
- Evolving Therapeutic Strategies in ANCA-Associated Vasculitis: Current Standards and Emerging Targets for GPA and MPA.Clinical reviews in allergy & immunology · 2026Review
- The Complement System in ANCA-Associated Vasculitis: Mechanistic Insights, Therapeutic Horizons, and Unmet Clinical Needs.Immunity, inflammation and disease · 2026Review
- Complement and immunoglobulin profiles in ANCA-associated vasculitis with renal involvement: a serotype-stratified analysis of disease activity and renal outcomes.Frontiers in immunology · 2026Article
- Targeting the complement system in ANCA-associated vasculitis management.Rheumatology (Oxford, England) · 2026Review
- Chimeric autoantibody receptor T cells for targeted depletion of myeloperoxidase-specific anti-neutrophil cytoplasmic antibody-producing B cells.Frontiers in immunology · 2026Article
- ANCA-associated vasculitis: a phase-oriented therapeutic framework from immunopathology to precision treatment.Frontiers in medicine · 2026Review
- Making use of avacopan in clinical practice.Clinical kidney journal · 2026Review
210 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Clinical and experimental data indicate that anti-neutrophil cytoplasmic autoantibodies (ANCAs) cause glomerulonephritis and vasculitis. Here we report the first evidence that complement is an important mediator of ANCA disease. Transfer of anti-myeloperoxidase (MPO) IgG into wild-type mice or anti-MPO splenocytes into immune-deficient mice caused crescentic glomerulonephritis that could be completely blocked by complement depletion. The role of specific complement activation pathways was investigated using mice with knockout of the common pathway component C5, classic and lectin binding pathway component C4, and alternative pathway component factor B. After injection of anti-MPO IgG, C4-/- mice developed disease comparable with wild-type disease; however, C5-/- and factor B-/- mice developed no disease. To substantiate a role for complement in human ANCA disease, IgG was isolated from patients with myeloperoxidase ANCA (MPO-ANCA) or proteinase 3 ANCA (PR3-ANCA) and from controls. Incubation of MPO-ANCA or PR3-ANCA IgG with human neutrophils caused release of factors that activated complement. IgG from healthy controls did not produce this effect. The findings suggest that stimulation of neutrophils by ANCA causes release of factors that activate complement via the alternative pathway, thus initiating an inflammatory amplification loop that mediates the severe necrotizing inflammation of ANCA disease.
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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.