ArticleProceedings of the National Academy of Sciences of the United States of America2017
Properdin binding to complement activating surfaces depends on initial C3b deposition.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.
- Therapeutic Targeting of the Complement System: From Rare Diseases to Pandemics.Pharmacological reviews · 2021Pooled it
- Complement Dysregulation in Kidney Diseases: Mechanisms, Biomarkers, and Emerging Targeted Therapies.International journal of molecular sciences · 2026Review
- Structural studies offer a framework for understanding the role of properdin in the alternative pathway and beyond.Immunological reviews · 2023Review
- Initial properdin binding contributes to alternative pathway activation at the surface of viable and necrotic cells.European journal of immunology · 2022Article
- Article
- Modeling C3 glomerulopathies: C3 convertase regulation on an extracellular matrix surface.Frontiers in immunology · 2022Article
- The Contribution of Complement to the Pathogenesis of IgA Nephropathy: Are Complement-Targeted Therapies Moving from Rare Disorders to More Common Diseases?Journal of clinical medicine · 2021Review
- Targeting complement components C3 and C5 for the retina: Key concepts and lingering questions.Progress in retinal and eye research · 2021Review
- Systems Biology Modeling of the Complement System Under Immune Susceptible Pathogens.Frontiers in physics · 2021Article
- More than a Pore: Nonlytic Antimicrobial Functions of Complement and Bacterial Strategies for Evasion.Microbiology and molecular biology reviews : MMBR · 2021Review
- Renal diseases and the role of complement: Linking complement to immune effector pathways and therapeutics.Advances in immunology · 2021Review
- Article
- Clinical and functional consequences of anti-properdin autoantibodies in patients with lupus nephritis.Clinical and experimental immunology · 2020Article
- Properdin Pattern Recognition on Proximal Tubular Cells Is Heparan Sulfate/Syndecan-1 but Not C3b Dependent and Can Be Blocked by Tick Protein Salp20.Frontiers in immunology · 2020Article
- The Role of Properdin in Killing of Non-PathogenicFrontiers in immunology · 2020Article
- The Interplay Between Blood Proteins, Complement, and Macrophages on Nanomedicine Performance and Responses.The Journal of pharmacology and experimental therapeutics · 2019Review
- The role of properdin in complement-mediated renal diseases: a new player in complement-inhibiting therapy?Pediatric nephrology (Berlin, Germany) · 2019Article
- New insights into the immune functions of complement.Nature reviews. Immunology · 2019Review
- Novel insights into the treatment of complement-mediated hemolytic anemias.Therapeutic advances in hematology · 2019Review
- Structural Basis for Properdin Oligomerization and Convertase Stimulation in the Human Complement System.Frontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Two functions have been assigned to properdin; stabilization of the alternative convertase, C3bBb, is well accepted, whereas the role of properdin as pattern recognition molecule is controversial. The presence of nonphysiological aggregates in purified properdin preparations and experimental models that do not allow discrimination between the initial binding of properdin and binding secondary to C3b deposition is a critical factor contributing to this controversy. In previous work, by inhibiting C3, we showed that properdin binding to zymosan and Escherichia coli is not a primary event, but rather is solely dependent on initial C3 deposition. In the present study, we found that properdin in human serum bound dose-dependently to solid-phase myeloperoxidase. This binding was dependent on C3 activation, as demonstrated by the lack of binding in human serum with the C3-inhibitor compstatin Cp40, in C3-depleted human serum, or when purified properdin is applied in buffer. Similarly, binding of properdin to the surface of human umbilical vein endothelial cells or Neisseria meningitidis after incubation with human serum was completely C3-dependent, as detected by flow cytometry. Properdin, which lacks the structural homology shared by other complement pattern recognition molecules and has its major function in stabilizing the C3bBb convertase, was found to bind both exogenous and endogenous molecular patterns in a completely C3-dependent manner. We therefore challenge the view of properdin as a pattern recognition molecule, and argue that the experimental conditions used to test this hypothesis should be carefully considered, with emphasis on controlling initial C3 activation under physiological conditions.
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