Guillain-Barré syndrome and anti-ganglioside antibodies: A clinician-scientist’s journey
Open accessAbstract
Guillain-Barré syndrome (GBS) is the most frequent cause of acute flaccid 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 identified 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 review, I wanted 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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Flagged first, then by citations
Research works printed but not linked: 2
- [56]Asbury A.K. Cornblath D.R. (1998) Preserved tendon reflexes in Campylobacter neuropathy: reply. Ann. Neurol. 43, 547 9546342
- [75]Yuki N. Susuki K. Koga M. Nishimoto Y. Kamijo M. (2002) Myelin-derived glycolipids and animal models of Guillain–Barré syndrome: reply. Ann. Neurol. 51, 532– 533 11921062
Cited by
Sorted by citations
Schnaar, R. L., Gerardy-Schahn, R., & Hildebrandt, H. (2014) · Physiological Reviews · doi:10.1152/physrev.00033.2013 · Cited by 745 · see citing works
De Masi, R., & Orlando, S. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23137373 · Cited by 20 · see citing works
“Sci. 2022, 23, 7373 31 of 49 DD disease duration; DMF Dimethyl Fumarate; DMT disease modifying therapy; DNJ 1-deoxynojirimycin; EAE experimental allergic encephalitis; ER endoplasmic reticulum; ERAD ER-associated degradation; ERGIC ER-Golgi intermediate compartment; FAD flavin adenine inucleotide; GADD34 growth arrest…”
Background
- Authors
- YUKI, N.
- Affiliations
- National University of Singapore (SG)
- Corresponding author
- YUKI, Nobuhiro
- ORCID
- YUKI, Nobuhiro
- Venue
- Proceedings of the Japan Academy Series B
- Publisher
- Japan Academy
- Published
- 2012
- Volume
- 88
- Issue
- 7
- Pages
- 299-326
- ISSN
- 0386-2208 (ISSN-L)
- 1349-2896
- PMC
- PMC3422685
- OpenAlex
- W1550227150
- Cited by
- 109
- References
- 193
- Citations by year
- 2026: 3 · 2025: 12 · 2024: 10 · 2023: 5 · 2022: 7 · 2021: 10 · 2020: 12 · 2019: 7 · 2018: 4 · 2017: 5 · 2016: 11 · 2015: 11 · 2014: 8 · 2013: 4
- FWCI
- 1.03
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the Japan Academy Series B (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- National University of Singapore (submittedVersion)
- Funders
- Dokkyo Medical University
- Universiti Malaya
- Chiba University
- National Research Council Canada
- Topics
- Health Sciences › Medicine › Neurology › Peripheral Neuropathies and Disorders
- Health Sciences › Medicine › Neurology › Autoimmune Neurological Disorders and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Hereditary Neurological Disorders
- Keywords
- Guillain-Barré syndrome, anti-ganglioside antibodies, GM1 ganglioside, Campylobacter jejuni, molecular mimicry, lipooligosaccharide, Miller Fisher syndrome, Bickerstaff brainstem encephalitis, anti-GQ1b antibodies, autoimmune disease pathogenesis, acute flaccid paralysis, disease models
- MeSH terms
- Animals, Antibodies, Gangliosides, Humans, Research Personnel, Miller Fisher Syndrome, Guillain-Barre Syndrome, Biomedical Research
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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