ArticleClinical and experimental immunology2008
Neutrophil surface presentation of the anti-neutrophil cytoplasmic antibody-antigen proteinase 3 depends on N-terminal processing.
Article in Clinical and experimental immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Dipeptidyl peptidase 1 inhibition as a potential therapeutic approach in neutrophil-mediated inflammatory disease.Frontiers in immunology · 2023Review
- Inflammatory Proteins HMGA2 and PRTN3 as Drivers of Vulvar Squamous Cell Carcinoma Progression.Cancers · 2020Article
- Kidney injury enhances renal G-CSF expression and modulates granulopoiesis and human neutrophil CD177 in vivo.Clinical and experimental immunology · 2020Article
- Proteinase 3 expression on the neutrophils of patients with paroxysmal nocturnal hemoglobinuria.Experimental and therapeutic medicine · 2018Article
- Gene silencing and a novel monoallelic expression pattern in distinct CD177 neutrophil subsets.The Journal of experimental medicine · 2017Article
- Gene-Specific DNA Methylation Changes Predict Remission in Patients with ANCA-Associated Vasculitis.Journal of the American Society of Nephrology : JASN · 2017Article
- Characterization of the CD177 interaction with the ANCA antigen proteinase 3.Scientific reports · 2017Article
- Impaired phagocytosis and reactive oxygen species production in phagocytes is associated with systemic vasculitis.Arthritis research & therapy · 2016Article
- Neutrophil proteinase 3 and dipeptidyl peptidase I (cathepsin C) as pharmacological targets in granulomatosis with polyangiitis (Wegener granulomatosis).Seminars in immunopathology · 2013Review
- How anti-neutrophil cytoplasmic autoantibodies activate neutrophils.Clinical and experimental immunology · 2012Review
- Loss of expression of neutrophil proteinase-3: a factor contributing to thrombotic risk in paroxysmal nocturnal hemoglobinuria.Haematologica · 2011Article
- Complement receptor Mac-1 is an adaptor for NB1 (CD177)-mediated PR3-ANCA neutrophil activation.The Journal of biological chemistry · 2011Article
- Neutrophil elastase, proteinase 3, and cathepsin G as therapeutic targets in human diseases.Pharmacological reviews · 2010Review
- The use of small molecule high-throughput screening to identify inhibitors of the proteinase 3-NB1 interaction.Clinical and experimental immunology · 2010Article
- An approach to the diagnosis and management of systemic vasculitis.Clinical and experimental immunology · 2010Review
- Catalytic activity and inhibition of wegener antigen proteinase 3 on the cell surface of human polymorphonuclear neutrophils.The Journal of biological chemistry · 2009Article
- Translational mini-review series on immunology of vascular disease: mechanisms of vascular inflammation and remodelling in systemic vasculitis.Clinical and experimental immunology · 2009Review
- Update on pathogenic mechanisms of systemic necrotizing vasculitis.Current rheumatology reports · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The neutrophil serine protease proteinase 3 (PR3) is a main autoantigen in anti-neutrophil cytoplasmic antibody-associated vasculitis. PR3 surface presentation on neutrophilic granulocytes, the main effector cells, is pathogenically important. PR3 is presented by the NB1 (CD177) glycoprotein, but how the presentation develops during neutrophil differentiation is not known. An N-terminally unprocessed PR3 (proPR3) is produced early during neutrophil development and promotes myeloid cell differentiation. We therefore investigated if PR3 presentation depended on NB1 during neutrophil differentiation and if PR3 and proPR3 could both be presented by NB1. In contrast to mature neutrophils, differentiating neutrophils showed an early NB1-independent PR3 surface display that was recognized by only two of four monoclonal anti-PR3 antibodies and occurred in parallel with proPR3, but not PR3 secretion, suggesting that the NB1-independent surface PR3 was proPR3. PR3 gene expression preceeded NB1. When the NB1 receptor was detected on the surface, a mode of PR3 surface display similar to mature neutrophils developed together with the degranulation system. Ectopic expression studies showed that NB1 was a sufficient receptor for PR3 but not proPR3. ProPR3 display on the plasma membrane may influence the bone marrow microenvironment. NB1-mediated PR3 presentation depended on PR3 N-terminal processing implicating the PR3-N-terminus as NB1-binding site.
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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.