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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2008-6-23
pubmed:abstractText
The Guillain Barré syndromes (GBS) are the world's leading cause of acute autoimmune neuromuscular paralysis. Understanding the pathophysiological events of GBS, and improving immunotherapies are fundamental to improving the clinical outcome. Recent research into GBS and the Miller Fisher syndrome (MFS) variant has focused on the forms mediated by anti-ganglioside antibodies in which correlations have been established between anti-ganglioside antibodies and specific clinical phenotypes, notably between anti-GM1/GD1a antibodies and the acute motor axonal variant and anti-GQ1b/GT1a antibodies and MFS. Anti-ganglioside antibodies can arise through molecular mimicry with GBS-associated Campylobacter jejuni oligosaccharides. Our work has focused on axonal and glial components of the motor nerve terminal as a model site of injury, and through combined active and passive immunization paradigms in glycosyltransferase knockout mice we have developed murine neuropathy phenotypes mediated by anti-ganglioside antibodies. Several determinants influence disease expression including the level of immunological tolerance to microbial glycans that mimic self gangliosides, the degree of complement activation, and the ganglioside density in target tissue. Such studies provide us with clear information on an antibody-mediated pathogenesis model for GBS and should lead to rational therapeutic testing of agents that are potentially suitable for use in man.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0077-8923
pubmed:author
pubmed:issnType
Print
pubmed:volume
1132
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
114-23
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Anti-ganglioside antibodies and the presynaptic motor nerve terminal.
pubmed:affiliation
Division of Clinical Neurosciences, University of Glasgow , Scotland, UK. h.j.willison@clinmed.gla.ac.uk
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't