| Project/Area Number |
61571108
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Laboratory medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
TAKIGUCHI Masafumi M.D. Assistant Professor, Institute of Medical Science, University of Tokyo, 医科学研究所, 助手 (00183450)
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| Co-Investigator(Kenkyū-buntansha) |
KANO Kyoichi M.D. Professor, Institute of Medical Science, University of Tokyo, 医科学研究所, 教授 (80152825)
ARIGA Hiroyoshi PhD Assistant Professor, Institute of Medical Science, University of Tokyo, 医科学研究所, 助手 (20143505)
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| Project Period (FY) |
1986 – 1987
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1987: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1986: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | novel HLA class I gene / Qa gene / Qa遺伝子 / HLA抗原 / HLAC-Blank遺伝子 / 主要組織適合抗原 |
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| Research Abstract |
We tried the cloning of novel HLA calss I genes by (1) the probe of 190bp mouse Q4 specific DNA or (2) the probe of HLA B7 cDNA. Several kinds of clone which hybridized with the probe (1) were cloned and all of them were transfected into mouse L cells. No HLA class I antigens on all L cell transformants was detected by the flowcytometry assay with mouse anti-HLS class I monoclonal antibodies (mAbs). On the other hand, six kinds of HLA class I genes from the library of normal peripheral blood lymphocyte (HLA-All/24, B52/52, Cw7/-) and two kinds of HLA class I genes from the library of homozygote cell line LKT-2 (HLA-A2/2. B51/51, C-/-) were isolated by the probe (2). All of them were expressed on mouse L cells. HLA-All, A24, B52, Cw7, B51 genes were determined by the absorption of corresponding alloantisera by these gene products on L cells. The remaining two genes were thougth to be C-blank gene because EchRI fragment was 7.6Kb and the binding of W6/32 mAb on these genes transfected L cells was weak.
The sequence data of C-blank gene from LKT-2 demonstrated that this gene resembled Cw1, but apparently was different from those of Cw1, Cw2 and Cw3. Only five amino acid differences (three on _1 domain and two on _2 domain) was observed between this gene and Cw1. These differences of aminoacid on _1 and _2 domain may make the novel alloantegeneicity.
The sequence experiments of another C-blank gene and an unidentified class i gene is under investigation.
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