ArticleClinical and experimental immunology1995
Proteolysis of classic anti-neutrophil cytoplasmic autoantibodies (C-ANCA) by neutrophil proteinase 3.
Article in Clinical and experimental immunology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Activation of a Latent Epitope Causing Differential Binding of Antineutrophil Cytoplasmic Antibodies to Proteinase 3.Arthritis & rheumatology (Hoboken, N.J.) · 2023Article
- Membrane-Associated Proteinase 3 on Granulocytes and Acute Myeloid Leukemia Inhibits T Cell Proliferation.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Proteinase 3 Induces Neuronal Cell Death Through Microglial Activation.Neurochemical research · 2015Article
- Proteinase 3 contributes to transendothelial migration of NB1-positive neutrophils.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Alternative complement pathway induction by ANCA.The American journal of pathology · 2008Article
- Agreement of anti-neutrophil cytoplasmic antibody measurements obtained from serum and plasma.Clinical and experimental immunology · 2006Article
- B cell epitope specificity in ANCA-associated vasculitis: does it matter?Clinical and experimental immunology · 2004Review
- Interference of PR3-ANCA with the enzymatic activity of PR3: differences in patients during active disease or remission of Wegener's granulomatosis.Clinical and experimental immunology · 2002Article
- What you should know about PR3-ANCA. An introduction.Arthritis research · 2000Review
- Characterization of monoclonal antibodies to proteinase 3 (PR3) as candidate tools for epitope mapping of human anti-PR3 autoantibodies.Clinical and experimental immunology · 1999Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C-ANCA, which are directed against neutrophil proteinase 3 (PR3), are specific markers for the diagnosis of active Wegener's granulomatosis (WG). The correlation between C-ANCA titre and WG disease activity suggests that these autoantibodies are involved in the development of WG. We have previously observed that C-ANCA interfere with PR3 proteolytic activity and with complexation of PR3 with its major physiologic inhibitor alpha 1-antitrypsin (alpha 1-AT). The possible pathogenic importance of C-ANCA may be related to the stability of C-ANCA IgG-PR3 complexes. In the present study we tested proteolysis by PR3 of human IgG and proteolysis of C-ANCA IgG complexed to the enzyme. All human IgG subclass proteins were cleaved by PR3. Digestion products were compared with those obtained by human neutrophil elastase (HNE)-mediated proteolysis of human IgG subclass proteins. Although cleavage products of similar size could be identified, the proteolytic activity of both enzymes towards human IgG differed. Furthermore, inhibiting C-ANCA IgG were cleaved into small peptides when complexed to PR3. The possible pathogenic consequences of these findings will be discussed.
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