Molecular mimicry as a mechanism of autoimmune disease

Matthew F. Cusick, Jane E. Libbey, Robert S. Fujinami*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

337 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)102-111
Number of pages10
JournalClinical Reviews in Allergy and Immunology
Issue number1
StatePublished - Feb 2012


  • Autoimmune diseases
  • Dual T cell receptor
  • Immunopathology
  • Molecular mimicry
  • Virus infection

ASJC Scopus subject areas

  • Immunology and Allergy


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