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Experimental approach in research of Guillain–Barré syndrome: A range of pathogeneses mediated by molecular mimicry
Author(s) -
Koga Michiaki
Publication year - 2018
Publication title -
clinical and experimental neuroimmunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.297
H-Index - 15
ISSN - 1759-1961
DOI - 10.1111/cen3.12457
Subject(s) - molecular mimicry , campylobacter jejuni , mycoplasma pneumoniae , pathogenesis , immunology , biology , mimicry , cytomegalovirus , autoantibody , virus , virology , medicine , antibody , herpesviridae , genetics , pneumonia , viral disease , bacteria , ecology
Molecular mimicry between microbial antigens and host tissue is a highly attractive explanation for the pathogenesis of many autoimmune diseases. Among them, Guillain–Barré syndrome ( GBS ) is an excellent model to show the causal pathogenesis of molecular mimicry, because the epidemiological association of GBS with several infections has been established. The present review describes recent findings regarding the causative role of molecular mimicry in GBS that arises after infection with several different bacteria and viruses, including Campylobacter jejuni , Mycoplasma pneumoniae , cytomegalovirus, Haemophilus influenzae , Epstein–Barr virus, hepatitis E virus and Zika virus. Although many issues must be resolved to fully understand GBS pathogenesis, molecular mimicry is highly likely to be involved in the development of C. jejuni ‐associated GBS and probably of M. pneumoniae ‐associated GBS . Candidate autoantibodies that are generated in cytomegalovirus‐ and H. influenzae ‐associated GBS types can also provide clues to the causal role of molecular mimicry. For other diseases associated with antecedent infections, clarification of pathogeneses is premature and warrants further research on molecular mimicry, as well as other autoimmune‐triggering mechanisms.