Format

Send to

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

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

Author information

1
Department of Pharmaceutical Biotechnology and Pharmaceutical Sciences Research Center, Faculty of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran.
2
Department of Pharmaceutical Biotechnology and Pharmaceutical Sciences Research Center, Faculty of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran; Faculty of Pahrmacy and Pharmaceutical Sciences, Hormozgan University of Medical Sciences, Bandar Abbas, Iran.
3
Department of Neurology, Shiraz University of Medical Sciences, Shiraz, Iran.
4
Department of Pharmaceutical Biotechnology and Pharmaceutical Sciences Research Center, Faculty of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran. Electronic address: ghasemiy@sums.ac.ir.

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)

PMID:
27235356
DOI:
10.1016/j.jneuroim.2016.03.018
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center