Document Detail

Tcell anergy as a strategy to reduce the risk of autoimmunity.
MedLine Citation:
PMID:  21354182     Owner:  NLM     Status:  Publisher    
Some self-reactive immature T cells escape negative selection in the thymus and may cause autoimmune diseases later. In the periphery, if T cells are stimulated insufficiently by peptide-major histocompatibility complex, they become inactive and their production of cytokines changes, a phenomenon called "T cell anergy". In this paper we explore the hypothesis that T cell anergy may function to reduce the risk of autoimmunity. The underlying logic is as follows: Since those self-reactive T cells that receive strong stimuli from self-antigens are eliminated in the thymus, T cells that receive strong stimuli in the periphery are likely to be non-self-reactive. As a consequence, when a T cell receives a weak stimulus, the likelihood that the cell is self-reactive is higher than in the case that it receives a strong stimulus. Therefore, inactivation of the T cell may reduce the danger of autoimmunity. We consider the formalism in which each T cell chooses its response depending on the strength of stimuli in order to reduce the risk of autoimmune diseases while maintaining its ability to attack non-self-antigens effectively. The optimal T cell responses to a weak and a strong stimulus are obtained both when the cells respond in a deterministic manner and when they respond in a probabilistic manner. We conclude that T cell anergy is the optimal response when a T cell meets with antigen-presenting cells many times in its lifetime, and when the product of the autoimmunity risk and the number of self-reactive T cells has an intermediate value.
Koichi Saeki; Yoh Iwasa
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-2-23
Journal Detail:
Title:  Journal of theoretical biology     Volume:  -     ISSN:  1095-8541     ISO Abbreviation:  -     Publication Date:  2011 Feb 
Date Detail:
Created Date:  2011-2-28     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0376342     Medline TA:  J Theor Biol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2011. Published by Elsevier Ltd.
Department of Biology, Faculty of Sciences, Kyushu University, Fukuoka 812-8581, Japan.
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