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Abstract Title:

Molecular mimicry as a mechanism of autoimmune disease.

Abstract Source:

Clin Rev Allergy Immunol. 2012 Feb ;42(1):102-11. PMID: 22095454

Abstract Author(s):

Matthew F Cusick, Jane E Libbey, Robert S Fujinami

Article Affiliation:

Matthew F Cusick

Abstract:

A variety of mechanisms have been suggested as the means by which infections can initiate and/or exacerbate autoimmune diseases. One mechanism is molecular mimicry, where a foreign antigen shares sequence or structural similarities with self-antigens. Molecular mimicry has typically been characterized on an antibody or T cell level. However, structural relatedness between pathogen and self does not account for T cell activation in a number of autoimmune diseases. A proposed mechanism that could have been misinterpreted for molecular mimicry is the expression of dual T cell receptors (TCR) on a single T cell. These T cells have dual reactivity to both foreign and self-antigens leaving the host vulnerable to foreign insults capable of triggering an autoimmune response. In this review, we briefly discuss what is known about molecular mimicry followed by a discussion of the current understanding of dual TCRs. Finally, we discuss three mechanisms, including molecular mimicry, dual TCRs, and chimeric TCRs, by which dual reactivity of the T cell may play a role in autoimmune diseases.

Study Type : Review

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Sayer Ji
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