| Project/Area Number |
01480296
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Hematology
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| Research Institution | University of Tokyo |
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Principal Investigator |
MINAMI Matsuhiko University of Tokyo, Dept Transfusionn Medicine, Associate Professor, 医学部(病), 助教授 (60092342)
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| Co-Investigator(Kenkyū-buntansha) |
TAKIGUCHI Masafumi University of Tokyo, Dept Immunology, Assistant Professor, 医科学研究所, 助手 (00183450)
JUJI Takeo University of Tokyo, Dept Transfusionn Medicine, Professor, 医学部(病), 教授 (20009997)
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| Project Period (FY) |
1989 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥6,800,000 (Direct Cost: ¥6,800,000)
Fiscal Year 1990: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1989: ¥5,000,000 (Direct Cost: ¥5,000,000)
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| Keywords | GVH / MHC / minor histocompatibility / CTL / HLA / T cell receptor / alloreactive T cell / 細胞障害性T細胞 / イディオタイプ / Adhesion molecule / CD2 / ICAM-1 / トランスジェニックマウス |
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| Research Abstract |
The project suppored by this grant intended to clarify mechanisms of induction of graft-versus-host (GVH) diseases. The clarification is required for establishment of methods for prevention or therapy of GVH diseases. We did the following subjects ; 1) analysis of major histocompatibility complex (MHC) molecules, especially HLA class I molecules, 2) analysis of minor histocompatibility (mH) antigenic system in human, and 3) finally suppression of alloreactive T cells inducing GVH diseases. First, we analyzed molecular structure and molecular evolution on HLA-B51 and B52, HLA-B35 and HLA-C molecules. Further, from the peripheral blood lymphocytes of a patient with kidney transplantation, we established cytotoxic T cell clones responding to a type of mH antigen on the cells of the patient. The CTL clones could kill HLA-B35-positive cells without expression of the type of mH antigen in the presence of the peptide (s) eluted from the cells of the patient. Also, from the transfused patient we established T cell clone reacting to mH antigen in a HLA-DR9-restricted manner. Finally, in the serum of a multitransfused patient we detected and characterized antibodies reacting to T cell receptors expressed on the T cells reacting to allo-HLA expressed on the patient.
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