| Project/Area Number |
14570581
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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 | Kinki University (2003)
The University of Tokyo (2002) |
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Principal Investigator |
KUSUNOKI Susumu Kinki University School of Medicine, Department of Neurology, Professor and Chairman, 医学部, 教授 (90195438)
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| Co-Investigator(Kenkyū-buntansha) |
等 誠司 東京大学, 医学部附属病院, 教務職員 (70300895)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2003: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2002: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Guillain-Barre syndrome / ganglioside / phospholipid / CIDP / neuroimmunology / glycolipid / neuropathy / antiganglioside antibody / ギラン・バレー症候群 / 自己免疫 / ニューロパケー / 脱髄 |
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| Research Abstract |
Antiganglioside antibodies are useful diagnostic markers of autoimmune neuropathies. They may be involved in the pathogenetic mechanisms as well. Gangliosides in the cell membrare are surrounded by phospholipids. We investigated serum antibody activities against a mixture of a ganglioside and a phospholipid. The reactivities of the anti-GM1 IgG antibodies in Guillain-Barre syndrome(GBS) were enhanced by the use of a mixture antigen of GM1 and such a phospholipid as PA,PS and PI. Such an enhancement was not seen for the anti-GQ1b IgG antibodies in Miller Fisher syndrome. The reactivates of both of those antibodies were reduced by the addition of SM. The reactivities of the anti-GM1 IgM antibodies in autoimmune neuropathies such as GBS, chronic inflammatory demyelinating polyradiculoneuropathy, and multifocal motor neuropathy were not enhanced by the addition of such a phospholiid as PA,PS and PI to the antigen mixture, while those were reduced by the addition of SM. The effect of SM that decreases the reactivities of the antiganglioside antibodies in autoimmune neuropathies may be the reason why an antiganglioside antibody does not cause ubiquitous damage on the neurological system but affects only the place where the ganglioside is densely localized. The binding activities of the anti-GalNAc-GD1a IgG antibodies were enhanced by the addition of PA to die antigen mixture. This resembles the results on the anti-GM1 IgG antibodies as described above. This may be due to the fact that both of the antibodies are associated with die preceding Campylobacter jejuni infection. Our results suggest that we should pay more attention to the effect by the phospholipids when we consider the role of the antiganglioside antibodies in the pathogenetic mechanisms. Similar investigation is needed on the serum antibodies in the neuroimmunological diseases other than autoimmune neuropathies.
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