ArticleJournal of theoretical biology2015
Continuum model of T-cell avidity: Understanding autoreactive and regulatory T-cell responses in type 1 diabetes.
Article in Journal of theoretical biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 2 of them syntheses that pooled it.
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Who cites it
10 citing papers in PubMed, 2 syntheses or guidelines pooled it, 20 citations in OpenAlex.
- Clinical parameters and emerging biomarkers of partial remission in pediatric type 1 diabetes: a systematic review.Frontiers in endocrinology · 2026Pooled it
- Mathematical modeling in autoimmune diseases: from theory to clinical application.Frontiers in immunology · 2024Pooled it
- Chronic infection control relies on T cells with lower foreign antigen binding strength generated by N-nucleotide diversity.PLoS biology · 2024Article
- Candidate Biomarkers for the Prediction and Monitoring of Partial Remission in Pediatric Type 1 Diabetes.Frontiers in immunology · 2022Article
- Hybrid computational modeling demonstrates the utility of simulating complex cellular networks in type 1 diabetes.PLoS computational biology · 2021Article
- Quantifying immunoregulation by autoantigen-specific T-regulatory type 1 cells in mice with simultaneous hepatic and extra-hepatic autoimmune disorders.Immunology · 2020Article
- The Remission Phase in Type 1 Diabetes: Role of Hyperglycemia Rectification in Immune Modulation.Frontiers in endocrinology · 2019Review
- miRNAs: novel regulators of autoimmunity-mediated pancreatic β-cell destruction in type 1 diabetes.Cellular & molecular immunology · 2017Review
- Liraglutide Enhances the Efficacy of Human Mesenchymal Stem Cells in Preserving Islet β-cell Function in Severe Non-obese Diabetic Mice.Molecular medicine (Cambridge, Mass.) · 2016Article
- Spatiotemporal Dynamics of Insulitis in Human Type 1 Diabetes.Frontiers in physiology · 2016Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Type 1 diabetes (T1D) is an autoimmune disease that results from the destruction of insulin-secreting pancreatic β cells, leading to abolition of insulin secretion and onset of diabetes. Cytotoxic CD4(+) and CD8(+) T cells, activated by antigen presenting cells (APCs), are both implicated in disease onset and progression. Regulatory T cells (Tregs), on the other hand, play a leading role in regulating immunological tolerance and resistant homoeostasis in T1D by suppressing effector T cells (Teffs). Recent data indicates that after activation, conventional Teffs transiently produce interleukin IL-2, a cytokine that acts as a growth factor for both Teffs and Tregs. Tregs suppress Teffs through IL-2 deprivation, competition and Teff conversion into inducible Tregs (iTregs). To investigate the interactions of these components during T1D progression, a mathematical model of T-cell dynamics is developed as a predictor of β-cell loss, with the underlying hypothesis that avidity of Teffs and Tregs, i.e., the binding affinity of T-cell receptors to peptide-major histocompatibility complexes on host cells, is continuum. The model is used to infer a set of criteria that determines susceptibility to T1D in high risk subjects. Our findings show that diabetes onset is guided by the absence of Treg-to-Teff dominance at specific high avidities, rather than over the whole range of avidity, and that the lack of overall dominance of Teffs-to-Tregs over time is the underlying cause of the "honeymoon period", the remission phase observed in some T1D patients. The model also suggests that competition between Teffs and Tregs is more effective than Teff-induction into iTregs in suppressing Teffs, and that a prolonged full width at half maximum of IL-2 release is a necessary condition for curbing disease onset. Finally, the model provides a rationale for observing rapid and slow progressors of T1D based on modest heterogeneity in the kinetic parameters.
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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.