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- Vol.41 No.12
- CLINICA NEUROL, 41: 1141－1143, 2001
- Vol.41 No.12 contents
The 42nd Annual Meeting of the Japanese Society of Neurology
Symposium VIII-1: Immunological disorders in nervous system
Pathogenetic mechanisms of autoimmune neuropathies caused by antiglycolipid antibodies
Susumu Kusunoki, M. D.
Department of Neurology, School of Medicine, University of Tokyo
Antiglycolipid antibody titers are frequently elevated in the serum of patients with autoimmune neuropathies. Some antibodies may be involved in the pathogenesis because glycolipids are surface antigens in the nervous system. Sensory ataxic neuropathy was induced in rabbits sensitized with GD1b ganglioside, which is localized in the rabbit primary sensory neurons of the larger cytoplasms. Systemic infusion of high-titer anti-GD1b antiserum to rabbits pre-inoculated with adjuvant caused vacuolar degeneration with macrophage infiltration in a few axons in the dorsal column of the spinal cord. Anti-GD1b antibody therefore may cause degeneration in rabbit sensory neurons with central axons extending to the dorsal column. Investigations on the clinical features of GBS patients with monospecific anti-GD1b IgG antibodies showed that the antibodies are associated with sensory disturbance, especially disturbance in the deep sensation, and with primary demyelinating form. GD1b is localized in primary sensory neurons and paranodal myelin in the human peripheral nervous system. Monospecific anti-GD1b IgG antibodies may bind to those regions and be involved in the pathogenesis of sensory disturbance and demyelination. Thus, some antiglycolipid antibodies may determine the clinical features of GBS by binding to the regions where the antigens are localized.
(CLINICA NEUROL, 41: 1141－1143, 2001)
key words: Guillain-Barré syndrome, autoimmune neuropathies, gangliosides, glycolipids, ataxia
(Received: 13-May-01)
