A theory of immunodominance and adaptive regulation

DOI10.1007/S11538-010-9585-5MaRDI QIDQ644582zbMATHOpenAlexWikidataFDO

Authors Peter S. Kim, Peter P. Lee, Doron Levy

Publication date 4 November 2011

Published in Bulletin of Mathematical Biology (Search for Journal in Brave)

Full work available at URL http://europepmc.org/articles/pmc3865720

zbMATH Keywords

delay differential equationscompetition modeladaptive regulatory T cellsT cell response

Mathematics Subject Classification ID

Medical applications (general) (92C50) Dynamical systems in biology (37N25) Probabilistic models, generic numerical methods in probability and statistics (65C20) Physiology (general) (92C30) Qualitative investigation and simulation of models involving functional-differential equations (34K60) Cell biology (92C37)

Recommendations

• Basic Principles in Modeling Adaptive Regulation and Immunodominance
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• Epitope down-modulation as a mechanism for the coexistence of competing T-cells
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Cites work

• Emergent group dynamics governed by regulatory cells produce a robust primary T cell response

Cited in

(13)

• Basic Principles in Modeling Adaptive Regulation and Immunodominance
• Functional switching and stability of regulatory T cells
• Epitope down-modulation as a mechanism for the coexistence of competing T-cells
• Modeling LSD1-mediated tumor stagnation
• Mathematical modeling of humoral immune response suppression by passively administered antibodies in mice
• Modeling immunodominance in the B-cell response to viral infection
• Modeling the effect of memory in the adaptive immune response
• Modeling the development of cellular exhaustion and tumor-immune stalemate
• A stability theorem for equilibria of delay differential equations in a critical case with application to a model of cell evolution
• The role of antigen-competitive dynamics in regulating the immune response
• A Regulatory Principle for Robust Reciprocal-Time Decay of the Adaptive Immune Response
• Immunodominance analysis through interactions of CD8\(^+\) T cells and DCs in lymph nodes
• Targeting CD4+ T cell exhaustion to improve future immunotherapy strategies

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