ArticleFrontiers in immunology2013
A mathematical model of immune activation with a unified self-nonself concept.
Article in Frontiers in immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mathematical modeling in autoimmune diseases: from theory to clinical application.Frontiers in immunology · 2024Pooled it
- A biological and a mathematical model of SLE treated by mesenchymal stem cells covering all the stages of the disease.Theory in biosciences = Theorie in den Biowissenschaften · 2023Article
- Article
- An Adaptive Control Scheme for Interleukin-2 Therapy.iScience · 2020Article
- Endocrine Autoimmune Disease as a Fragility of Immune Surveillance against Hypersecreting Mutants.Immunity · 2020Article
- Quantitative Mechanistic Modeling in Support of Pharmacological Therapeutics Development in Immuno-Oncology.Frontiers in immunology · 2019Review
- Stochastic modeling of tumor progression and immune evasion.Journal of theoretical biology · 2018Article
- Importance of Feedback and Feedforward Loops to Adaptive Immune Response Modeling.CPT: pharmacometrics & systems pharmacology · 2018Review
- Integrating Immunology and Microfluidics for Single Immune Cell Analysis.Frontiers in immunology · 2018Review
- A Dynamic Model of Immune Responses to Antigen Presentation Predicts Different Regions of Tumor or Pathogen Elimination.Cell systems · 2017Article
- Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The adaptive immune system reacts against pathogenic nonself, whereas it normally remains tolerant to self. The initiation of an immune response requires a critical antigen(Ag)-stimulation and a critical number of Ag-specific T cells. Autoreactive T cells are not completely deleted by thymic selection and partially present in the periphery of healthy individuals that respond in certain physiological conditions. A number of experimental and theoretical models are based on the concept that structural differences discriminate self from nonself. In this article, we establish a mathematical model for immune activation in which self and nonself are not distinguished. The model considers the dynamic interplay of conventional T cells, regulatory T cells (Tregs), and IL-2 molecules and shows that the renewal rate ratio of resting Tregs to naïve T cells as well as the proliferation rate of activated T cells determine the probability of immune stimulation. The actual initiation of an immune response, however, relies on the absolute renewal rate of naïve T cells. This result suggests that thymic selection reduces the probability of autoimmunity by increasing the Ag-stimulation threshold of self reaction which is established by selection of a low number of low-avidity autoreactive T cells balanced with a proper number of Tregs. The stability analysis of the ordinary differential equation model reveals three different possible immune reactions depending on critical levels of Ag-stimulation: a subcritical stimulation, a threshold stimulation inducing a proper immune response, and an overcritical stimulation leading to chronic co-existence of Ag and immune activity. The model exhibits oscillatory solutions in the case of persistent but moderate Ag-stimulation, while the system returns to the homeostatic state upon Ag clearance. In this unifying concept, self and nonself appear as a result of shifted Ag-stimulation thresholds which delineate these three regimes of immune activation.
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