ArticleProceedings of the National Academy of Sciences of the United States of America2021
Tregs self-organize into a computing ecosystem and implement a sophisticated optimization algorithm for mediating immune response.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 0 citations in OpenAlex.
- Central T cell tolerance from sparse peptide sampling.Science advances · 2026Article
- Article
- Dynamical model and geometric insights in the discontinuity theory of immunity.bioRxiv : the preprint server for biology · 2025Article
- Affinity maturation for an optimal balance between long-term immune coverage and short-term resource constraints.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The evolution of powerful yet perilous immune systems.Trends in immunology · 2022Review
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
Regulatory T cells (Tregs) play a crucial role in mediating immune response. Yet an algorithmic understanding of the role of Tregs in adaptive immunity remains lacking. Here, we present a biophysically realistic model of Treg-mediated self-tolerance in which Tregs bind to self-antigens and locally inhibit the proliferation of nearby activated T cells. By exploiting a duality between ecological dynamics and constrained optimization, we show that Tregs tile the potential antigen space while simultaneously minimizing the overlap between Treg activation profiles. We find that for sufficiently high Treg diversity, Treg-mediated self-tolerance is robust to fluctuations in self-antigen concentrations but lowering the Treg diversity results in a sharp transition-related to the Gardner transition in perceptrons-to a regime where changes in self-antigen concentrations can result in an autoimmune response. We propose an experimental test of this transition in immune-deficient mice and discuss potential implications for autoimmune diseases.
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