Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2009-6-1
pubmed:abstractText
The neuromuscular junction lies beyond the protection of the blood-brain barrier and is particularly vulnerable to antibody-mediated attack. In myasthenia gravis, the expression of acetylcholine receptors (AChRs) in the thymus is under the control of the autoimmune regulator protein (AIRE), and polymorphisms in the AChR correlate with early onset of disease. In some 'AChR seronegative' patients, thymic abnormalities associated with complement-activating antibodies binding only clustered AChRs have been demonstrated, and in others anti-muscle-specific kinase (MuSK) antibodies that show pathogenic effects in vivo. In Guillain-Barré syndrome, newly described antibodies bind to complex gangliosides. General immunosuppression is still the main treatment, but novel treatments that reduce complement-mediated damage or inhibit the binding of pathogenic antibodies are beginning to look promising.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1471-4892
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
336-40
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Autoimmune disorders of the neuromuscular junction.
pubmed:affiliation
Department of Clinical Neurology, University of Oxford, Oxford OX3 9DS, UK. blang@hammer.imm.ox.ac.uk
pubmed:publicationType
Journal Article, Review