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神経科学学会-神経学会合同シンポジウム:Neuroimmunology Cutting Edge Symposium: Mechanisms of Immune-mediated Neurological Disease
Joint Symposium of the Japan Neuroscience Society and the Japanese Society of Neurology:Neuroimmunology Cutting Edge Symposium:
Mechanisms of Immune-mediated Neurological Disease

開催日 2014/9/13
時間 9:00 - 11:00
会場 Room A(Main Hall)
Chairperson(s) 吉良 潤一 / Jun-ichi Kira (九州大学大学院医学系研究院 神経内科学 / Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Japan)
神田 隆 / Takashi Kanda (山口大学大学院医学系研究科神経内科学 / Department of Neurology and Clinical Neuroscience, Yamaguchi University Graduate School of Medicine, Japan)

Guillain-Barré syndrome and anti-ganglioside antibodies: a clinician-scientist’s journey

  • S3-A-1-2
  • 結城 伸泰 / Nobuhiro Yuki:1 
  • 1:シンガポール国立大学、シンガポール / Dept Med, National University of Singapore, Singapore 

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

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