Bioinformatics evaluation of the possibility of heat shock proteins as autoantigens in multiple sclerosis based on molecular mimicry hypothesis

J Neuroimmunol. 2016 Jun 15:295-296:100-21. doi: 10.1016/j.jneuroim.2016.03.018. Epub 2016 Apr 9.

Abstract

Molecular mimicry is the explanatory link between the heat shock proteins (HSPs) of infectious agents and triggering multiple sclerosis. Considering that there are many similarities between self- and bacterial-HSPs, the goal was to investigate a panel of 60- and 70kDa HSPs from a variety of bacteria in order to predict the role of each microorganism in triggering or progression of the disease under the molecular mimicry hypothesis. By clarifying the peptides meeting criteria for cross-reactivity and elucidating the role of each microorganism in MS pathogenesis, it would be easier to suggest more effective treatment and preventive strategies for this disease.

Keywords: Autoimmunity; Heat shock proteins (HSPs); Immunoinformatics; Molecular mimicry; Multiple Sclerosis (MS).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Autoantigens / immunology*
  • Bacterial Proteins / immunology
  • Bacterial Proteins / metabolism
  • Computational Biology*
  • Cross Reactions
  • Heat-Shock Proteins / immunology*
  • Humans
  • Immunodominant Epitopes
  • Molecular Mimicry*
  • Molecular Weight
  • Multiple Sclerosis / immunology*
  • Multiple Sclerosis / metabolism*
  • Sequence Analysis, Protein

Substances

  • Autoantigens
  • Bacterial Proteins
  • Heat-Shock Proteins
  • Immunodominant Epitopes