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A bioinformatics analysis reveals novel pathogens as molecular mimicry triggers of systemic sclerosis

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Autore
Gkoutzourelas A., Barmakoudi M., Bogdanos D.P.
Data
2020
Language
en
DOI
10.31138/MJR.31.1.50
Soggetto
autoantibody
autoantigen
centromere antibody
centromere protein B
DNA topoisomerase
epitope
fibrillarin
Acinetobacter baumannii
Article
B lymphocyte
Bacillus
Bacillus paralicheniformis
bioinformatics
blood sampling
computer model
cross reaction
DNA virus
human
Human immunodeficiency virus 1
in vitro study
Klebsiella pneumoniae
Mastadenovirus
molecular mimicry
Paenibacillus
pathogenesis
Picornaviridae
sequence alignment
systemic sclerosis
Greek Rheumatology Society and Professional Association of Rheumatologists
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Abstract
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. © Gkoutzourelas A, Barmakoudi M, Bogdanos DP.
URI
http://hdl.handle.net/11615/72527
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  • Δημοσιεύσεις σε περιοδικά, συνέδρια, κεφάλαια βιβλίων κλπ. [19743]
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