Research article

Affinity and avidity models in autoimmune disease

  • 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.

    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

    Related Papers:

  • 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.


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  • © 2018 the Author(s), licensee AIMS Press. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0)
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