A Bioinformatics Analysis Reveals Novel Pathogens as Molecular Mimicry Triggers of Systemic Sclerosis

A recent bioinformatic analysis revealing dominant B cell epitopes of systemic sclerosis-specific autoantibodies, including anti-centromere B, anti-topoisomerase I and anti-fibrillarin, has demonstrated the existence of several in silico antigenic mimics of pathogens that could act as triggers of th...

Full description

Bibliographic Details
Main Authors: Athanasios Gkoutzourelas, Maria Barmakoudi, Dimitrios P. Bogdanos
Format: Article
Language:English
Published: PCO Convin S.A. 2019-01-01
Series:Mediterranean Journal of Rheumatology
Subjects:
Online Access:http://www.mjrheum.org/assets/files/792/file207_1089.pdf
id doaj-6f0cadf99d7a4d87931f62e1a5fb16c2
record_format Article
spelling doaj-6f0cadf99d7a4d87931f62e1a5fb16c22020-11-25T03:29:39ZengPCO Convin S.A.Mediterranean Journal of Rheumatology2529-198X2019-01-01311507010.31138/mjr.31.1.50MJR-31-1-50A Bioinformatics Analysis Reveals Novel Pathogens as Molecular Mimicry Triggers of Systemic SclerosisAthanasios Gkoutzourelas0Maria Barmakoudi1Dimitrios P. Bogdanos2Department of Rheumatology and Clinical Immunology, Faculty of Medicine, University of Thessaly, Larissa, GreeceDepartment of Rheumatology and Clinical Immunology, Faculty of Medicine, University of Thessaly, Larissa, GreeceDepartment of Rheumatology and Clinical Immunology, Faculty of Medicine, University of Thessaly, Larissa, GreeceA recent bioinformatic analysis revealing dominant B cell epitopes of systemic sclerosis-specific autoantibodies, including anti-centromere B, anti-topoisomerase I and anti-fibrillarin, has demonstrated the existence of several in silico antigenic mimics of pathogens that could act as triggers of the respective dominant autoepitopes. Based on those findings, the aim of the present study was to use a more comprehensive bioinformatic analysis. We demonstrated the presence of a plethora of novel microbial mimics, unnoticed by the studies so far conducted, which share remarkable amino acid similarities with the respective autoantigenic epitopes. This bioinformatic approach coupled by in vitro testing of the homologous self/non-self-mimics in serum samples from patients with systemic sclerosis may provide novel evidence of immunological cross-reactivity, implicating currently ignored or overlooked pathogens, which may indeed play a role in the induction of SSc-specific autoantibodies and assist efforts to understand the pathogenesis of this enigmatic disease.http://www.mjrheum.org/assets/files/792/file207_1089.pdfautoantibodyautoimmunityautoimmune rheumatic diseasesinfectionmolecular mimicry
collection DOAJ
language English
format Article
sources DOAJ
author Athanasios Gkoutzourelas
Maria Barmakoudi
Dimitrios P. Bogdanos
spellingShingle Athanasios Gkoutzourelas
Maria Barmakoudi
Dimitrios P. Bogdanos
A Bioinformatics Analysis Reveals Novel Pathogens as Molecular Mimicry Triggers of Systemic Sclerosis
Mediterranean Journal of Rheumatology
autoantibody
autoimmunity
autoimmune rheumatic diseases
infection
molecular mimicry
author_facet Athanasios Gkoutzourelas
Maria Barmakoudi
Dimitrios P. Bogdanos
author_sort Athanasios Gkoutzourelas
title A Bioinformatics Analysis Reveals Novel Pathogens as Molecular Mimicry Triggers of Systemic Sclerosis
title_short A Bioinformatics Analysis Reveals Novel Pathogens as Molecular Mimicry Triggers of Systemic Sclerosis
title_full A Bioinformatics Analysis Reveals Novel Pathogens as Molecular Mimicry Triggers of Systemic Sclerosis
title_fullStr A Bioinformatics Analysis Reveals Novel Pathogens as Molecular Mimicry Triggers of Systemic Sclerosis
title_full_unstemmed A Bioinformatics Analysis Reveals Novel Pathogens as Molecular Mimicry Triggers of Systemic Sclerosis
title_sort bioinformatics analysis reveals novel pathogens as molecular mimicry triggers of systemic sclerosis
publisher PCO Convin S.A.
series Mediterranean Journal of Rheumatology
issn 2529-198X
publishDate 2019-01-01
description A recent bioinformatic analysis revealing dominant B cell epitopes of systemic sclerosis-specific autoantibodies, including anti-centromere B, anti-topoisomerase I and anti-fibrillarin, has demonstrated the existence of several in silico antigenic mimics of pathogens that could act as triggers of the respective dominant autoepitopes. Based on those findings, the aim of the present study was to use a more comprehensive bioinformatic analysis. We demonstrated the presence of a plethora of novel microbial mimics, unnoticed by the studies so far conducted, which share remarkable amino acid similarities with the respective autoantigenic epitopes. This bioinformatic approach coupled by in vitro testing of the homologous self/non-self-mimics in serum samples from patients with systemic sclerosis may provide novel evidence of immunological cross-reactivity, implicating currently ignored or overlooked pathogens, which may indeed play a role in the induction of SSc-specific autoantibodies and assist efforts to understand the pathogenesis of this enigmatic disease.
topic autoantibody
autoimmunity
autoimmune rheumatic diseases
infection
molecular mimicry
url http://www.mjrheum.org/assets/files/792/file207_1089.pdf
work_keys_str_mv AT athanasiosgkoutzourelas abioinformaticsanalysisrevealsnovelpathogensasmolecularmimicrytriggersofsystemicsclerosis
AT mariabarmakoudi abioinformaticsanalysisrevealsnovelpathogensasmolecularmimicrytriggersofsystemicsclerosis
AT dimitriospbogdanos abioinformaticsanalysisrevealsnovelpathogensasmolecularmimicrytriggersofsystemicsclerosis
AT athanasiosgkoutzourelas bioinformaticsanalysisrevealsnovelpathogensasmolecularmimicrytriggersofsystemicsclerosis
AT mariabarmakoudi bioinformaticsanalysisrevealsnovelpathogensasmolecularmimicrytriggersofsystemicsclerosis
AT dimitriospbogdanos bioinformaticsanalysisrevealsnovelpathogensasmolecularmimicrytriggersofsystemicsclerosis
_version_ 1724577890301902848