2001 Fiscal Year Final Research Report Summary
Development of axonal degeneration by passive transfer of antiganglioside antibody and therapeutic trial for it.
| Project/Area Number |
12670595
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
KUSUNOKI Susumu Department of Neurology, The University of Tokyo, Assistant Professor and Lecturer, 医学部・附属病院, 講師 (90195438)
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| Project Period (FY) |
2000 – 2001
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| Keywords | Guillain-Barre syndrome. / ganglioside / neuropathy / autoimmunity / glycolipid / neuroimmunology / ataxia / demyelination |
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| Research Abstract |
We previously reported the development of sensory ataxic neuropathy (SAN) in rabbits sensitized with GD 1b ganglioside. To investigate the pathogenetic role of anti-GD 1b antibody, we performed intravenous infusion of anti-GD 1b antiserum from the affected rabbits into normal rabbits. It produced axonal degeneration with macrophage infiltration in primary sensory neurons with central axons extending to the dorsal column, the same pathological findings for GD 1b-induced SAN, showing that anti-GD 1b antibody is an important pathogenetic factor in this animal model Guillain-Barre syndrome (GBS) with monospecific IgG anti-GD 1b antibody was associated with disturbance in deep sensation and demyelinating form. GD 1b is localized in large primary sensory neurons and paranodal myelin. Monospecific anti-GD 1b antibody may bind to those regions and cause the above clinical features. Anti-Gal-C antibodies are present in the acute-phase sera from GBS patients subsequent to M. pneumoniae. We showed that a Gal-C-like structure is present in M. pneumoniae, indicative of molecular mimicry between a major myelin glycolipid, Gal-C, and M. pneumoniae.
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Research Products
(12 results)
