| Project/Area Number |
09558099
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | Tokyo Metropolitan Institute of Medical Science |
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Principal Investigator |
TAI Tadashi The Tokyo Metropolitan Organization of Medical Science, Tokyo Metropolitan Institute of Medical Science, Department of Tumor Immunology, Researcher, 東京都臨床医学総合研究所, 研究員 (70112092)
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| Co-Investigator(Kenkyū-buntansha) |
YONEKAWA Hiromichi The Tokyo Metropolitan Organization of Medical Science, Tokyo Metropolitan Institute of Medical Science, Vice president, 東京都臨床医学総合研究所, 副所長 (30142110)
KARASUYAMA Hajime The Tokyo Metropolitan Organization of Medical Science, Tokyo Metropolitan Institute of Medical Science, Department of Tumor Immunology, Researcher, 東京都臨床医学総合研究所, 研究員 (60195013)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1999: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1998: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | monoclonal antibody / carbohydrate chain / ganglioside / transgenic mouse / auto-immune disease / neuropathy |
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| Research Abstract |
The aim of the project is to establish model mice for auto-immune neuropathy by transfection with anti-carbohydrate antibody genes. A hybridoma producing a monoclonal antibody, which reacts specifically with b-pathway gangliosides such as GD3, GD2, GD1b, GT1b, and GQ1b, but not with any other gangliosides or neutral glycosphingolipids was selected among a series of hybridomas secreting monoclonal antibodies specific for carbohydrate chains, that were established in our laboratory. We generated, at first, transgenic mice having high antibody titer of IgM to the ganglioides. These mice appeared to be healthy and exhibited no significant pathological symptoms at 1-year-old. Next, we tried to induce neuropathy by immunizing these transgenic mice with a number of adjuvants including LPS and cytokines. However, they showed no significant symptoms. These results suggest that only high antibody titer to the gangliosides in sera is not enough for inducing neuronal symptoms. Further study will be needed for analyzing the mechanisms of the neuropathy. At present, we are producing transgenic mice having high antibody titer of IgG.
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