Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1990-8-8
pubmed:abstractText
In certain patients with demyelinating neuropathy and plasma cell dyscrasia, there are IgM monoclonal antibodies that recognize a carbohydrate epitope shared by myelin-associated glycoprotein (MAG) and at least two acidic glycolipids in the peripheral nervous system (PNS). The structures of the two acidic lipids have been elucidated as a new class of glycosphingolipids, termed sulfoglucuronyl glycolipids (SGGLs). SGGLs have been demonstrated to be present in myelin, axolemma, and other glia-related membranes in PNS of several animal species, as well as in human dorsal root ganglia and sympathetic ganglia. In rabbits sensitized with sulfoglucuronyl paragloboside (SGPG), a major SGGL in PNS, antibodies developed with reactivities toward SGPG and MAG. The animals also showed moderate weakness, a slowed nerve conduction velocity, and evidence of conduction block. Recently we also found SGPG in rat brain microvessels. This finding supports our hypothesis that autoantibodies may first interact with endothelial cell-bound antigens and that this might change the permeability of the blood-brain or blood-nerve barrier to permit the entry of these autoantibodies into the nervous system. Our data are consistent with the concept that an autoimmune response against the sulfoglucuronyl residue may participate in the pathogenesis of immune-mediated neuropathy.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0364-5134
pubmed:author
pubmed:issnType
Print
pubmed:volume
27 Suppl
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S30-5
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Autoimmune mechanisms in peripheral neuropathies.
pubmed:affiliation
Department of Biochemistry and Molecular Biophysics, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298-0614.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review