The role of molecular mimicry in the etiology of Guillain Barré Syndrome

Abstract

Molecular mimicry between host tissue structures and microbial components has been proposed as the pathogenic mechanism for triggering of autoimmune diseases by preceding infection. Recent studies stated that molecular mimicry as the causative mechanism remains unproven for most of the human diseases. Still, in the case of the peripheral neuropathy Guillain-Barré syndrome (GBS) this hypothesis is supported by abundant experimental evidence. GBS is the most frequent cause of acute neuromuscular paralysis and in some cases occurs after infection with Campylobacter jejuni (C. jejuni). Epidemiological studies, showed that more than one third of GBS patients had antecedent C. jejuni infection and that only specific C. jejuni serotypes are associated with development of GBS. The molecular mimicry between the human gangliosides and the core oligosaccharides of bacterial lipopolysaccharides (LPSs) presumably results in production of antiganglioside cross-reactive antibodies which are likely to be a contributory factor in the induction and pathogenesis of GBS. Antiganglioside antibodies were found in the sera from patients with GBS and by sensitization of rabbits with gangliosides and C. jejuni LPSs animal disease models of GBS were established. GBS as prototype of post-infection immune-mediated disease probably will provide the first verification that an autoimmune disease can be triggered by molecular mimicry.