ArticleBulletin of mathematical biology2020
Mathematical Modelling of Alternative Pathway of Complement System.
Article in Bulletin of mathematical biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.
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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
7 citing papers in PubMed.
- Safety, Tolerability, Pharmacokinetics, Pharmacodynamics, and Immunogenicity of ALXN1820 (Tarperprumig) in Healthy Adults: Results of a Phase I Study.Clinical and translational science · 2025Trial
- De-stabilizing innate immunity in COVID-19: effects of its own positive feedback and erratic viraemia on the alternative pathway of complement.Royal Society open science · 2024Article
- Unravelling the impact of SARS-CoV-2 on hemostatic and complement systems: a systems immunology perspective.Frontiers in immunology · 2024Article
- Vitamin D deficiency leads to the abnormal activation of the complement system.Immunologic research · 2023Article
- Article
- Systems Biology Modeling of the Complement System Under Immune Susceptible Pathogens.Frontiers in physics · 2021Article
- Modeling the activation of the alternative complement pathway and its effects on hemolysis in health and disease.PLoS computational biology · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The complement system (CS) is an integral part of innate immunity and can be activated via three different pathways. The alternative pathway (AP) has a central role in the function of the CS. The AP of complement system is implicated in several human disease pathologies. In the absence of triggers, the AP exists in a time-invariant resting state (physiological steady state). It is capable of rapid, potent and transient activation response upon challenge with a trigger. Previous models of AP have focused on the activation response. In order to understand the molecular machinery necessary for AP activation and regulation of a physiological steady state, we built parsimonious AP models using experimentally supported kinetic parameters. The models further allowed us to test quantitative roles played by negative and positive regulators of the pathway in order to test hypotheses regarding their mechanisms of action, thus providing more insight into the complex regulation of AP.
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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.