Molecular Mimicry: Infection-Inducing Autoimmune Disease

Volume 296 of the series Current Topics in Microbiology and Immunology pp 1-17

Molecular Mimicry, Microbial Infection, and Autoimmune Disease: Evolution of the Concept

  • M. B. A. OldstoneAffiliated withDivision of Virology, Departments of Neuropharmacology and Infectology, The Scripps Research Institute

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Molecular mimicry is defined as similar structures shared by molecules from dissimilar genes or by their protein products. Either several linear amino acids or their conformational fit may be shared, even though their origins are separate. Hence, during a viral or microbe infection, if that organism shares cross-reactive epitopes for B or T cells with the host, then the response to the infecting agent will also attack the host, causing autoimmune disease. A variation on this theme is when a second, third, or repeated infection(s) shares cross-reactive B or T cell epitopes with the first (initiating) virus but not necessarily the host. In this instance, the secondary infectious agents increase the number of antiviral/antihost effector antibodies or T cells that potentiate or precipitate the autoimmune assault. The formation of this concept initially via study of monoclonal antibody or clone T cell cross-recognition in vitro through its evolution to in vivo animal models and to selected human diseases is explored in this mini-review.