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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2008-6-23
pubmed:abstractText
Antibodies to muscle-specific kinase (MuSK) are found in a variable proportion of patients with myasthenia without typical acetylcholine receptor (AChR) antibodies, but their characteristics and pathogenic mechanisms are not fully understood. We discuss the incidence and pathogenicity of MuSK antibodies and how clinical studies, animal models, and cultured cell lines can be used to elucidate their pathogenic mechanisms. Patients without either AChR or MuSK antibodies (seronegative myasthenia) appear to present another disease subtype that is highly similar to that of typical myasthenia gravis. We demonstrate a new method that detects AChR antibodies in these patients and show that these low-affinity AChR antibodies are predominantly IgG1 and can activate complement C3b deposition. Similarly MuSK antibodies, although mainly IgG4, are partially IgG1 and can activate C3b deposition. Overall, these results suggest that complement-activation may be an important pathogenic mechanism even in patients without conventional AChR antibodies.
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
84-92
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Myasthenia gravis seronegative for acetylcholine receptor antibodies.
pubmed:affiliation
Neurosciences Group, Weatherall Institute of Molecular Medicine and Department of Clinical Neurology, John Radcliffe Hospital, Oxford, United Kingdom. angela.vincent@imm.ox.ac.uk
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't