作者: Nobuhiro YUKI
DOI: 10.2183/PJAB.88.299
关键词:
摘要: Guillain-Barre syndrome (GBS) is the most frequent cause of acute flaccid paralysis. Having seen my first GBS patient in 1989, I have since then dedicated time research towards understanding pathogenesis GBS. Along with several colleagues, we identified IgG autoantibodies against ganglioside GM1 two patients subsequent to Campylobacter jejuni enteritis. We proceeded demonstrate molecular mimicry between and bacterial lipo-oligosaccharide C. isolated from a Our group established disease model for by sensitization or GM1-like lipo-oligosaccharide. With this, new paradigm that carbohydrate can autoimmune disorders was demonstrated, making proof disease. Patients Fisher syndrome, characterized ophthalmoplegia ataxia, develop after an infection jejuni. showed genetic polymorphism sialyltransferase, enzyme essential biosynthesis ganglioside-like lipo-oligosaccharides determines whether syndrome. This introduces another microbial determine clinical phenotype human diseases. Similarities presentation Bickerstaff brainstem encephalitis caused debate as they are fact same demonstrated anti-GQ1b antibodies were common both, suggesting part spectrum. followed this work clarifying nosological relationship various presentations within antibody In review, wanted share journey being clinician clinician-scientist hopes inspiring younger clinicians follow similar path.