TY - JOUR
T1 - Autoimmune mechanisms in peripheral neuropathies
AU - Yu, Robert K.
AU - Ariga, Toshio
AU - Kohriyama, Tatsuo
AU - Kusunoki, Susumu
AU - Maeda, Yasuhiro
AU - Miyatani, Nobuyuki
PY - 1990
Y1 - 1990
N2 - 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.
AB - 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.
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U2 - 10.1002/ana.410270709
DO - 10.1002/ana.410270709
M3 - Article
C2 - 2163594
AN - SCOPUS:0025339685
SN - 0364-5134
VL - 27
SP - S30-S35
JO - Annals of Neurology
JF - Annals of Neurology
IS - 1 S
ER -