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The immunopathogenesis of Miller Fisher syndrome.

Abstract：

: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 Campylobacter jejuni enteritis. Serostrains of C. jejuni 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.

journal_name

J Neuroimmunol

journal_title

Journal of neuroimmunology

authors

Willison HJ,O'Hanlon GM

doi

10.1016/s0165-5728(99)00213-1

subject

Has Abstract

pub_date

1999-12-01 00:00:00

pages

3-12

issue

1-2

eissn

0165-5728

issn

1872-8421

pii

S0165572899002131

journal_volume

100

pub_type

杂志文章,评审

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