Linked Life Data

17986149

Source:http://linkedlifedata.com/resource/pubmed/id/17986149

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2007-11-7
pubmed:abstractText
Immune responses directed towards gangliosides and their microbial mimics are important mediators of several subtypes of acute post-infectious autoimmune neuropathy, collectively referred to as the Guillain-Barré syndromes. In this diverse group of paralytic syndromes, the immunopathology is in a proportion of cases characterised by anti-ganglioside antibody deposits, accompanied by inflammatory destruction of both axonal and glial components within the PNS. By gaining an understanding of the immunological mechanisms underlying these pathological pathways, it should be possible to select the correct targets for therapeutic intervention. Recent years has seen particular progress in our understanding of the basis for, and immunological consequences of molecular mimicry between gangliosides and microbial glycans, the relationships between ganglioside antibody specificity and different clinical phenotypes of GBS, the pathological basis for antibody-mediated nerve injury and the testing of intervention strategies in pre-clinical models. The focus of this mini-review is to provide a brief background to this field, summarise a selection of recent highlights focused on our own research, identify areas of outstanding knowledge and present data that supports novel therapeutic approaches based on the latest experimental findings.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1471-4159
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
103 Suppl 1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
143-9
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Gangliosides as targets for autoimmune injury to the nervous system.
pubmed:affiliation
Division of Clinical Neurosciences, University of Glasgow, Scotland. h.j.willison@clinmed.gla.ac.uk
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't