| Project/Area Number |
09670334
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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 |
Immunology
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
UDAKA Keiko graduate school of Science, KYOTO UNIVERSITY assistant professor, 大学院・理学研究科, 助手 (40263066)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1998: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1997: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | MHC / peptide / T cell epitope / tumor antigen / affinity / specificity / recogrition / レパートリー / T細胞 / 抗原認識機構 |
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| Research Abstract |
1. Specificity analysis on a single molecular basis.
a. Positional scanning of MHC class I molecules.
Peptide binding specificity was analyzed for three MHC class 1 molecules with the use of peptide libraries (Data Base is in preparation for public release). Use and limit of using the library binding data for prediction of MHC binding peptides were revealed by synthesizing and testing the binding capacity of > 70 peptides.
b. Identification of epitope peptides.
MHC binding peptides were predicted in the sequence of a tumor antigen, hepatitis C virus and dystrophin, as a transplantation antigen by the above method and their antigenicity was identified by immunizing mice or PBMC from humans.
c. Production of soluble MHC class I molecules and a soluble TCR.
Extracellular portion of MHC class I molecules, a TOR were cloned and expressed in E.coli and Baculovirus.
2. Specificity analysis on a single cell basis.
A series of one amino acid substituted epitope peptides were designed. Weakly active peptides acted like antagonists during T cell recognition. Such activity was closely related to their ability to recruit CD8 molecules during recognition.
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