The immunopathogenesis of Miller Fisher syndrome

Willison, H.J. and O'Hanlon, G.M. (1999) The immunopathogenesis of Miller Fisher syndrome. Journal of Neuroimmunology, 100(1-2), pp. 3-12. (doi: 10.1016/S0165-5728(99)00213-1)

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Over the past decade, remarkable progress has been made in our understanding of the pathogenesis of Miller Fisher syndrome (MFS), a clinical variant of Guillain Barré syndrome (GBS). MFS comprises the clinical triad of ataxia, areflexia and ophthalmoplegia. It is associated with acute-phase IgG antibodies to GQ1b and GT1a gangliosides in over 90% of cases which are highly disease specific. Like GBS, MFS is a post-infectious syndrome following diverse infections, but particular attention has been paid to its association with <i>Campylobacter jejuni</i> enteritis. Serostrains of <i>C. jejuni</i> isolated from infected patients bear ganglioside-like epitopes in their lipopolysaccharide core oligosaccharides, which elicit humoral immune responses exhibiting molecular mimicry with GQ1b/GT1a gangliosides. These antibodies are believed to be the principal cause of the syndrome and physiological studies aimed at proving this have focused on the motor-nerve terminal as a potential site of pathogenic action. This review describes these findings and formulates a pathogenesis model based on our current state of knowledge.

Item Type:Articles
Glasgow Author(s) Enlighten ID:Willison, Professor Hugh
Authors: Willison, H.J., and O'Hanlon, G.M.
College/School:College of Medical Veterinary and Life Sciences > School of Infection & Immunity
Journal Name:Journal of Neuroimmunology
ISSN (Online):1872-8421

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