| Project/Area Number |
61480155
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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 |
Immunology
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| Research Institution | University of Tokyo |
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Principal Investigator |
ASANO Yoshihiro University of Tokyo, Associate Professor, 医学部, 助教授 (70114353)
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| Co-Investigator(Kenkyū-buntansha) |
TADA Tomio University of Tokyo, Professor, 医学部, 教授 (10009136)
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| Project Period (FY) |
1986 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥6,500,000 (Direct Cost: ¥6,500,000)
Fiscal Year 1988: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1987: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1986: ¥3,000,000 (Direct Cost: ¥3,000,000)
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| Keywords | Major histocompatibility complex (MHC) / I-J / T cell receptor (TcR) / Ca^<++> / Influx / 主要組織適合遺伝子複合体(MHC) / I-J / T細胞抗原レセプター / サプレッサーT細胞 / ヘルパーT細胞 / T細胞クロン / MHC拘束 / 放射線照射骨髄キメラ / T細胞認識 |
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| Research Abstract |
Monoclonal antibodies (mAb) against I-region-controlled epitopes expressed exclusively on mature functional T cells but not on B cells and macrophages (anti-Iat and anti-I-J) were found to inhibit class II MHC-restricted cell interactions in the immunological circuit. The present study was undertaken to analyze a mechanism of expression of Iat and I-J epitopes on T cells and to study a functional role of these molecules in immune regulation. Four essential findings were obtained: first, Iat/I-J epitopes undergo systematic alterations according to the environmental MHC in radiation bone marrow chimeras. Secondary, the I-J epitope is not an idiotypic determinant of T cell antigen-receptor (TcR) but is on a distinct molecule from TcR. Third, we have been able to identify the I-J molecule of cloned T cells by the specific immunoprecipitation. The I-J molecule detected is a 90K dimeric molecule composed of 45K glycopeptide subunits distinct from TcR or CD28. Finally, the cross-linking of I-J molecules with specific mAb resulted in the inhibition of Ca_<++> influx induced via the specific stimulation by antigen and MHC. These results indicated that I-J (probably Iat as well) is a T cell surface molecule that transduces a signal to regulate the hydrolysis of intracellular messengers of T cell activation induced via the TcR/T3 complex.
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