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Fig. 1. Molecular mimicry hypotheses for Guillain-Barré syndrome. Infection by
Campylobacter jejuni ( C . jejuni ) with a ganglioside GM1-like and GD1a-like structure on
its cell surface may induce anti-GM1, anti-GD1a, or anti-GM1/GD1a complex IgG in
some patients. Subsequently, with these antibodies binding to the GM1 or GD1a which are
expressed on motor nerves, the patients suffer from limb weakness. On the other hand, C.
jejuni that carries GT1a-like or GD1c-like oligosaccharides may raise the anti-GQ1b anti-
body production in GBS patients. Due to the distribution of GQ1b in oculomotor nerves
and primary sensory neurons, Fisher syndrome and related conditions could be found.
Antecedent Pathogens
GBS occurs subsequent to the infections
of these pathogens
Campylobacter jejuni
The epidemiological association of antecedent C. jejuni infection with GBS
has been established for over ten years. However, this relationship has
been dubitable owing to the fewer false-positives in cultured-confirmed
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