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Molecular mimicry and autoimmune thyroid disease.

Salvatore Benvenga1,2,3, Fabrizio Guarneri4

  • 1Department of Clinical and Experimental Medicine - Endocrinology, University of Messina, Messina, Italy.

Reviews in Endocrine & Metabolic Disorders
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Summary

Molecular mimicry, where microbes trigger autoimmunity, is common in autoimmune diseases but understudied in autoimmune thyroid disease. This research identifies new microbial candidates potentially triggering thyroid autoimmunity using bioinformatics.

Keywords:
Amino acid sequence homologyAutoimmune thyroid diseaseBioinformaticsMolecular mimicry

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Area of Science:

  • Immunology
  • Microbiology
  • Genetics
  • Bioinformatics

Background:

  • Molecular mimicry is a well-established mechanism by which microbes can evade immune responses and influence host metabolic pathways.
  • In susceptible individuals, molecular mimicry between microbial and human antigens can lead to autoimmunity.
  • While implicated in various autoimmune diseases, the role of molecular mimicry in autoimmune thyroid disease remains relatively unexplored.

Purpose of the Study:

  • To review the existing literature on the potential role of molecular mimicry in triggering autoimmune thyroid disease.
  • To investigate amino acid sequence homologies between microbial proteins and thyroid autoantigens using in silico methods.
  • To identify novel microbial candidates and molecular targets involved in the pathogenesis of autoimmune thyroid disease.

Main Methods:

  • Literature review on molecular mimicry and autoimmune thyroid disease.
  • In silico analysis of amino acid sequences to identify homologies between microbial proteins and thyroid autoantigens.
  • Assessment of potential pathogenetic relevance based on autoepitope overlap and HLA-DR binding motifs.

Main Results:

  • Previous bioinformatics data support the role of Borrelia, Yersinia, Clostridium botulinum, Rickettsia prowazekii, and Helicobacter pylori in triggering autoimmune thyroid disease.
  • New in silico findings suggest potential roles for Toxoplasma gondii, Bifidobacteria, Lactobacilli, Candida albicans, Treponema pallidum, and hepatitis C virus.
  • The study highlights the reliability of bioinformatics tools in predicting cross-reactivity and identifying candidate molecules for further experimental validation.

Conclusions:

  • Molecular mimicry is a plausible trigger for autoimmune thyroid disease, with several microbial agents identified as potential culprits.
  • Bioinformatics analysis provides a valuable approach to identify and prioritize candidate microbes and autoantigens for experimental investigation.
  • Further in vitro and in vivo studies are warranted to confirm the pathogenic significance of the identified microbial targets in autoimmune thyroid disease.