| Project/Area Number |
05044178
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| Research Category |
Grant-in-Aid for international Scientific Research
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| Allocation Type | Single-year Grants |
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| Section | Joint Research |
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
MATSUZAKI Goro Dept.Immunol., Med.Inst.Bioreg., Kyushu Univ. Assistant Professor, 生体防御医学研究所, 助手 (30229455)
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| Co-Investigator(Kenkyū-buntansha) |
IVANYI Juraj Medical Research Council, Tuberculosis and Related Infections Unit, Professor, 教授
JURAJ Ivanyi MRC, 結核および関連疾患部, 教授
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥5,000,000 (Direct Cost: ¥5,000,000)
Fiscal Year 1994: ¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1993: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | gammadeltaT cells / stress protein / bacterial infection / 自己反応性 / hsp60 |
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| Research Abstract |
We have reported that gammadeltaT cells reactive to stress protein increase at early stage of Listeriainfection. We also found that stress protein-reactive gammadeltaT cells increase in syngeneic mixed lymphocyte reaction (MLR). From the observations, we estimated that self stress protein/bacterial stress protein-cross reactive gammadeltaT cells increase after bacterial infection. Therefore we analyzed self-reactive gammadeltaT cells to know further characteristics of stress protein-reactive gammadeltaT cells.
We establisher 8 self-reactive gammadeltaT cell hybridomas. Four hybridomas expressed Vdelta5 and four hybridomas expressed Vdelta6. Response of seven out of eight self-reactive gammadeltaT cell hybridomas was blocked by anti stress protein (Hsp60) -monoclonal antibody ML30. Since response of gammadeltaT cell hybridomas with different T cell receptor was blocked with the ML30 antibody, we reasoned that Hsp60 molecule, but not ML30 epitope of Hsp60, participate in antigen recognition by the gammadeltaT cell hybridomas.
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