ArticleFrontiers in immunology2020
Properdin Is a Key Player in Lysis of Red Blood Cells and Complement Activation on Endothelial Cells in Hemolytic Anemias Caused by Complement Dysregulation.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Safety, Tolerability, Pharmacokinetics, Pharmacodynamics, and Immunogenicity of ALXN1820 (Tarperprumig) in Healthy Adults: Results of a Phase I Study.Clinical and translational science · 2025Trial
- Paroxysmal Nocturnal Hemoglobinuria: Unraveling Its Molecular Pathogenesis and Advancing Targeted Therapeutic Strategies.Diseases (Basel, Switzerland) · 2025Review
- Complement is activated in patients with acute chest syndrome caused by sickle cell disease and represents a therapeutic target.Science translational medicine · 2025Article
- Case Report: Possible C3 nephritic factor-driven complement-mediated severe hemolytic anemia and acute kidney injury in a child withFrontiers in immunology · 2025Article
- Pathogenesis of Anemia in Canine Babesiosis: Possible Contribution of Pro-Inflammatory Cytokines and Chemokines-A Review.Pathogens (Basel, Switzerland) · 2023Review
- The complement alternative pathway in paroxysmal nocturnal hemoglobinuria: From a pathogenic mechanism to a therapeutic target.Immunological reviews · 2023Review
- Intertwined pathways of complement activation command the pathogenesis of lupus nephritis.Translational research : the journal of laboratory and clinical medicine · 2022Review
- Review
- A novel assay that characterizes properdin function shows neutrophil-derived properdin has a distinct oligomeric distribution.Frontiers in immunology · 2022Article
- Mechanisms Driving Neutrophil-Induced T-cell Immunoparalysis in Ovarian Cancer.Cancer immunology research · 2021Observational
- Article
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
The complement system alternative pathway (AP) can be activated excessively in inflammatory diseases, particularly when there is defective complement regulation. For instance, deficiency in complement regulators CD55 and CD59, leads to paroxysmal nocturnal hemoglobinuria (PNH), whereas Factor H mutations predispose to atypical hemolytic uremic syndrome (aHUS), both causing severe thrombohemolysis. Despite eculizumab being the treatment for these diseases, benefits vary considerably among patients. Understanding the molecular mechanisms involved in complement regulation is essential for developing new treatments. Properdin, the positive AP regulator, is essential for complement amplification by stabilizing enzymatic convertases. In this study, the role of properdin in red blood cell (RBC) lysis and endothelial cell opsonization in these AP-mediated diseases was addressed by developing
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Registered trials
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