Reviews in Endocrine and Metabolic Disorders

, Volume 17, Issue 4, pp 485–498 | Cite as

Molecular mimicry and autoimmune thyroid disease

  • Salvatore Benvenga
  • Fabrizio GuarneriEmail author


Hypothesized 40 years ago, molecular mimicry has been thereafter demonstrated as an extremely common mechanism by which microbes elude immune response and modulate biosynthetic/metabolic pathways of the host. In genetically predisposed persons and under particular conditions, molecular mimicry between microbial and human antigens can turn a defensive immune response into autoimmunity. Such triggering role and its pathogenetic importance have been investigated and demonstrated for many autoimmune diseases. However, this is not the case for autoimmune thyroid disease, which appears relatively neglected by this field of research. Here we review the available literature on the possible role of molecular mimicry as a trigger of autoimmune thyroid disease. Additionally, we present the results of in silico search for amino acid sequence homologies between some microbial proteins and thyroid autoantigens, and the potential pathogenetic relevance of such homologies. Relevance stems from the overlap with known autoepitopes and the occurrence of specific HLA-DR binding motifs. Bioinformatics data published by our group support and explain the triggering role of Borrelia, Yersinia, Clostridium botulinum, Rickettsia prowazekii and Helicobacter pylori. Our new data suggest the potential pathogenic importance of Toxoplasma gondii, some Bifidobacteria and Lactobacilli, Candida albicans, Treponema pallidum and hepatitis C virus in autoimmune thyroid disease, indicating specific molecular targets for future research. Additionally, the consistency between in silico prediction of cross-reactivity and experimental results shows the reliability and usefulness of bioinformatics tools to precisely identify candidate molecules for in vitro and/or in vivo experiments, or at least narrow down their number.


Autoimmune thyroid disease Molecular mimicry Bioinformatics Amino acid sequence homology 


Compliance with ethical standards

Conflict of interest

The authors declare that they have no conflict of interest.


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© Springer Science+Business Media New York 2016

Authors and Affiliations

  1. 1.Department of Clinical and Experimental Medicine – EndocrinologyUniversity of MessinaMessinaItaly
  2. 2.Master Program on Childhood, Adolescent and Women’s Endocrine HealthUniversity of MessinaMessinaItaly
  3. 3.Interdepartmental Program on Molecular & Clinical Endocrinology and Women’s Endocrine HealthUniversity Hospital, Policlinico G. MartinoMessinaItaly
  4. 4.Department of Clinical and Experimental Medicine – DermatologyUniversity of MessinaMessinaItaly

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