Monoclonal antibodies raised against Guillain-Barré syndrome–associated Campylobacter jejuni lipopolysaccharides react with neuronal gangliosides and paralyze muscle-nerve preparations

AIDP and CIDP having specific antibodies to the carbohydrate epitope (–NeuAcα2–8NeuAcα2–3Galβ1–4Glc–) of gangliosides

“…GD3 is known to be a component of human peripheral nerve [30] and rat dorsal ganglion neurons [31]. Goodyear et al [32] reported the presence of GD3 epitope in NMJ and the effect of anti-GD3 antibody on the muscle action potential of NMJ. Accordingly anti-GD3 antibody may be associated with the demyelinating process by injuring Schwann cells in our cases.…”

The Guillain–Barré syndrome: a true case of molecular mimicry

“…These questions can be answered using large cohorts of welldefined GBS patients and careful analysis of GBS cases following outbreaks of Campylobacter infections [45]. New animal models for GBS Animal studies have shown that immunisation and infection with C. jejuni or purified LOS result in a crossreactive anti-ganglioside and LOS response [46,47]. As expected, the specificity of the anti-ganglioside antibodies in the animals was similar to the specificity in GBS patients from whom these Campylobacter strains were derived [46].…”

“…This forms strong evidence that the ganglioside autoantibodies in humans can be induced by molecular mimicry between Campylobacter LOS and gangliosides. The immunised and infected animals did not develop neuropathy but the anti-ganglioside antibodies generated in animals share pathogenic properties with human GBS sera [47]. Furthermore, immunisation of rabbits with purified gangliosides induces neurological disorders, some of which resemble GBS.…”

Variants of Guillain-Barré syndrome: low incidence but high impact

“…This was first demonstrated for the axonal GBS variants with the establishment of an epidemiological association with preceding Campylobacter jejuni infection and the occurrence of serum anti-ganglioside antibodies [7]. The discovery that these antibodies cross-react with ganglioside-like moieties on the surface of Campylobacter jejuni laid the foundations for the subsequent studies by Yuki and other groups [3,4,15,19,20] that provided support to the intriguing hypothesis of postinfectious molecular mimicry as a cause of GBS.…”