Affinity and avidity models in autoimmune disease

James Peterson; James Peterson

doi:10.3934/Allergy.2018.1.45

AIMS Allergy and Immunology

2018, Volume 2, Issue 1: 45-81. doi: 10.3934/Allergy.2018.1.45

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Research article

Affinity and avidity models in autoimmune disease

James Peterson ^,

Department of Mathematical Sciences, Clemson University, Clemson, SC 29634, USA

Received: 20 February 2018 Accepted: 27 March 2018 Published: 08 April 2018

In this work, we develop a theoretical model of affinity and avidity in the immune system.The model is based on an extension of the Cubic Ternary Complex (CTC) model of receptor - ligandinteractions to the immunological synapse setting. We use the resulting equation to study how lysiscan occur for a cell exhibiting only self proteins. This general affinity model gives a nice quantitativetool which can be used to explore a nonlinear model of how a T Cell can have a productive interactionwith a MHC-I complex even though the encapsulated peptide fragment is a self protein. The modelbuilt will allow the creation of even more general autoimmune models within the framework of B andT Cell differentiation via cytokine signalling families.
- T cell models,
- cubic ternary complex receptor,
- ligand interactions,
- immunological kinapses and synapses,
- self versus non-self computations,
- affinity,
- efficacy and avidity models
Citation: James Peterson. Affinity and avidity models in autoimmune disease[J]. AIMS Allergy and Immunology, 2018, 2(1): 45-81. doi: 10.3934/Allergy.2018.1.45

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Abstract

In this work, we develop a theoretical model of affinity and avidity in the immune system.The model is based on an extension of the Cubic Ternary Complex (CTC) model of receptor - ligandinteractions to the immunological synapse setting. We use the resulting equation to study how lysiscan occur for a cell exhibiting only self proteins. This general affinity model gives a nice quantitativetool which can be used to explore a nonlinear model of how a T Cell can have a productive interactionwith a MHC-I complex even though the encapsulated peptide fragment is a self protein. The modelbuilt will allow the creation of even more general autoimmune models within the framework of B andT Cell differentiation via cytokine signalling families.

References

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