ReviewSeminars in immunopathology2018
The properdin pathway: an "alternative activation pathway" or a "critical amplification loop" for C3 and C5 activation?
Review in Seminars in immunopathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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.
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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.
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Who cites it
36 citing papers in PubMed.
- Inflammatory involvement into phototoxic reaction in erythropoietic protoporphyria (EPP) patients.Immunologic research · 2019Trial
- Genetic Variation in the Alternative Complement Pathway Contributes to Individual Susceptibility to Bacteremia and Sepsis.Critical care explorations · 2025Article
- Cryo-EM analysis of complement C3 reveals a reversible major opening of the macroglobulin ring.Nature structural & molecular biology · 2025Article
- Native C3 is activated without proteolytic cleavage by transformation to C3(HFrontiers in immunology · 2025Article
- Mechanisms by which Factor H protectsFrontiers in immunology · 2024Article
- Complement and COVID-19: Three years on, what we know, what we don't know, and what we ought to know.Immunobiology · 2023Review
- Properdin inhibition ameliorates hepatic ischemia/reperfusion injury without interfering with liver regeneration in mice.Frontiers in immunology · 2023Article
- Alternative pathway activation: Ever ancient and ever new.Immunological reviews · 2023Review
- Genetic variability shapes the alternative pathway complement activity and predisposition to complement-related diseases.Immunological reviews · 2023Review
- Structural studies offer a framework for understanding the role of properdin in the alternative pathway and beyond.Immunological reviews · 2023Review
- Low-molecular weight inhibitors of the alternative complement pathway.Immunological reviews · 2023Review
- C3-dependent effector functions of complement.Immunological reviews · 2023Review
- Physiology and pathology of the C3 amplification cycle: A retrospective.Immunological reviews · 2023Review
- Exercise Promotes Bone Marrow Microenvironment by Inhibiting Adipsin in Diet-Induced Male Obese Mice.Nutrients · 2022Article
- Structure and function of a family of tick-derived complement inhibitors targeting properdin.Nature communications · 2022Article
- Complement-targeted therapies in kidney transplantation-insights from preclinical studies.Frontiers in immunology · 2022Review
- A novel assay that characterizes properdin function shows neutrophil-derived properdin has a distinct oligomeric distribution.Frontiers in immunology · 2022Article
- In silico analysis suggests disruption of interactions between HAMP from hepatocytes and SLC40A1 from macrophages in hepatocellular carcinoma.BMC medical genomics · 2021Article
- Nanobodies Provide Insight into the Molecular Mechanisms of the Complement Cascade and Offer New Therapeutic Strategies.Biomolecules · 2021Review
- Effect of red seaweed sulfated galactans on initial steps of complement activation in vitro.Carbohydrate polymers · 2021Article
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This review is not intended to cover in detail all aspects of the discovery and evolution of our understanding of the "alternative pathway" of complement activation, there are many excellent reviews that do this (see Fearon (CRC Crit Rev Immunol 1:1-32, 1979), Pangburn and Müller-Eberhard (Springer Semin Immunopathol 7:163-192, 1984)), but instead to give sufficient background for current concepts to be put in context. The prevailing textbook view, of components having a primary role as an alternative "pathway" for C3 activation, is challenged, with an argument developed for the primary role of the system being that of providing a surface-dependent amplification loop for both C3 and C5 activation. Whatever the mechanism by which the initial C3b molecule is generated, deposition onto a surface has the potential to target that surface for elimination. Elimination or escape from initial targeting is determined by a sophisticated and highly regulated amplification loop for C3 activation. This viewpoint of the system is then briefly developed to provide a context for therapeutic treatment of disease caused, at least in part, by dysregulated amplification of C3 activation, and to highlight some of the challenges that such therapies will face and need to address.
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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.