Autoimmune factors are strongly favoured as mediating Guillain-Barre s
yndrome (GBS); however, the precise mechanisms by which this occurs re
main unknown. Microbial infections in a susceptible host resulting in
an idiosyncratic immune response which cross-reacts with nerve constit
uents still remains the most plausible working hypothesis on which muc
h current research is based. Considerable recent evidence indicates th
at this humoral immune response is at least in part directed to gangli
osides. Interestingly, many bacterial toxins, including botulinum and
tetanus neurotoxins, also bind to gangliosides and induce diseases wit
h some similarities to GBS. This article discusses the evidence in fav
our of a pathogenic role for anti-ganglioside antibodies in GBS in the
context of our knowledge of the biology of gangliosides and the facto
rs that determine their immunogenicity.