ArticleJournal of innate immunity2014
Myeloperoxidase directs properdin-mediated complement activation.
Article in Journal of innate immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Therapeutic Targeting of the Complement System: From Rare Diseases to Pandemics.Pharmacological reviews · 2021Pooled it
- The Interaction of Neutrophil Extracellular Traps and Complement in Intracerebral Hemorrhage.Cellular and molecular neurobiology · 2026Review
- Salivary small extracellular vesicles reveal protein signatures in young patients with coronary artery disease.Clinical proteomics · 2025Article
- The Crosstalk Between NETs and the Complement Cascade: An Overview in Nephrological Autoimmune Disease.International journal of molecular sciences · 2025Review
- Immune-mediated mechanisms and maternal-fetal interface dysfunction in obstetric antiphospholipid syndrome.Frontiers in immunology · 2025Review
- Expression of Properdin, the positive regulator of the Complement Alternative Pathway, at the fetal-maternal interface in Preeclampsia.Frontiers in immunology · 2025Article
- Differential expression of complement Properdin and Factor H in the placentae and umbilical cords of mothers with Preeclampsia, Gestational Diabetes Mellitus and Recurrent Pregnancy Loss.Frontiers in immunology · 2025Article
- Circulating extracellular vesicles and neutrophil extracellular traps contribute to endothelial dysfunction in preeclampsia.Frontiers in immunology · 2024Article
- Anti-Neutrophil Extracellular Trap Antibodies in Antiphospholipid Antibody-Positive Patients: Results From the Antiphospholipid Syndrome Alliance for Clinical Trials and InternatiOnal Networking Clinical Database and Repository.Arthritis & rheumatology (Hoboken, N.J.) · 2023Article
- Crosstalk between neutrophil extracellular traps and immune regulation: insights into pathobiology and therapeutic implications of transfusion-related acute lung injury.Frontiers in immunology · 2023Review
- Effects of dietary supplementation ofFish and shellfish immunology reports · 2022Article
- Proteomic analysis identifies a signature of disease severity in the plasma of COVID-19 pneumonia patients associated to neutrophil, platelet and complement activation.Clinical proteomics · 2022Article
- Myeloperoxidase immunohistochemical staining can identify glomerular endothelial cell injury in dense deposit disease.Pediatric nephrology (Berlin, Germany) · 2021Article
- Hypocomplementemia at Diagnosis of Pauci-immune Glomerulonephritis Is Associated With Advanced Histopathological Activity Index and High Probability of Treatment Resistance.Kidney international reports · 2021Article
- Extracellular vesicles mediate cellular interactions in renal diseases-Novel views of intercellular communications in the kidney.Journal of cellular physiology · 2021Review
- Endothelial dysfunction and immunothrombosis as key pathogenic mechanisms in COVID-19.Nature reviews. Immunology · 2021Review
- The interplay between neutrophils, complement, and microthrombi in COVID-19.Best practice & research. Clinical rheumatology · 2021Review
- Article
- Inflammaging and Complement System: A Link Between Acute Kidney Injury and Chronic Graft Damage.Frontiers in immunology · 2020Review
- Mechanisms of haemolysis-induced kidney injury.Nature reviews. Nephrology · 2019Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophils and complement are key members of innate immunity. The alternative pathway (AP) of complement consists of C3, factor B, factor D and properdin, which amplifies AP activation. AP has been implicated in many neutrophil-mediated diseases, such as anti-neutrophil cytoplasmic antibody-associated vasculitis. The exact mechanism by which the AP and neutrophils interact remains largely unstudied. We investigated the ability of the AP to interact with neutrophil components which can be exposed and released upon activation. Our studies focused on neutrophil enzymes, including myeloperoxidase (MPO), proteinase 3 (PR3), azurocidin, elastase, lysozyme and cathepsin G. All enzymes except for azurocidin were able to bind properdin. However, only MPO could induce C3 activation. MPO mediated AP complement activation in the presence of MgEGTA compared to the EDTA control. This activation resulted in C3 deposition and required properdin to occur. Furthermore, we could show that MPO binds properdin directly, which then serves as a focus for AP activation. In summary, properdin can directly interact with neutrophil components. MPO demonstrates the ability to activate the AP which is dependent on properdin. Finally, MPO is capable of inducing properdin-initiated C3 and C5b-9 deposition in vitro.
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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.