ArticlePloS one2011
Reactivity against complementary proteinase-3 is not increased in patients with PR3-ANCA-associated vasculitis.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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Who cites it
11 citing papers in PubMed, 30 citations in OpenAlex.
- The Nasal Microbiome in ANCA-Associated Vasculitis: Picking the Nose for Clues on Disease Pathogenesis.Current rheumatology reports · 2021Review
- Human Proteinase 3, an important autoantigen of c-ANCA associated vasculitis, shares cross-reactive epitopes with serine protease allergens from mites: anF1000Research · 2021Article
- ANCA-associated vasculitis.Nature reviews. Disease primers · 2020Review
- ANCA-associated vasculitis - clinical utility of using ANCA specificity to classify patients.Nature reviews. Rheumatology · 2016Review
- Pathophysiological Relationship between Infections and Systemic Vasculitis.Autoimmune diseases · 2015Review
- The immunopathology of ANCA-associated vasculitis.Seminars in immunopathology · 2014Review
- The immune system and kidney disease: basic concepts and clinical implications.Nature reviews. Immunology · 2013Review
- Pathogenesis of ANCA-associated vasculitis.Current rheumatology reports · 2012Review
- Molecular recognition theory and sense-antisense interaction: therapeutic applications in autoimmunity.Frontiers in bioscience (Elite edition) · 2012Review
- Autoimmunity: Does autoantigen complementarity underlie PR3-ANCA AAV?Nature reviews. Rheumatology · 2011Article
- Pathogenesis of ANCA-associated vasculitis.Rheumatic diseases clinics of North America · 2010Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The etiology of anti-neutrophil cytoplasmic antibodies (ANCA) associated vasculitides (AAV) is unknown, but the association between infections and autoimmunity has been studied extensively. In 2004, a novel theory was proposed that could link infection and autoimmunity. This 'theory of autoantigen complementarity' was based on the serendipitous finding of antibodies against complementary-PR3 (cPR3) in patients with PR3-ANCA-associated vasculitis. cPR3 demonstrated homology to several bacterial proteins, and it was hypothesized that PR3-ANCA develop in response to anti-cPR3 antibodies, as a consequence of the anti-idiotypic network. These data have not been confirmed in other patient cohorts. We investigated the presence of anti-cPR3 antibodies in a Dutch cohort of PR3-ANCA-associated vasculitis patients. Anti-cPR3 reactivity was determined in serum using ELISA. Two separate batches of cPR3 were used to determine reactivity in two separate cohorts of PR3-ANCA-associated vasculitis patients. We found that anti-cPR3-reactivity was not increased in our PR3-ANCA-associated vasculitis patients, in comparison to control groups. Further research will be necessary to prove the concept of autoantigen complementarity in autoimmune diseases.
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