| Project/Area Number |
04454210
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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 |
免疫学
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| Research Institution | Okayama University |
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Principal Investigator |
NAKAYAMA Eiichi Okayama University Medical School, Professor, 医学部, 教授 (60180428)
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| Co-Investigator(Kenkyū-buntansha) |
ONO Toshiro Okayama University Medical School, Assistant Professor, 医学部, 助手 (50185641)
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1993: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | CTL / CD4^-CD8^-TCR alphabeta CTL / CD8-depletion / MHC class I antigen / MHC class I-restricted antigen / 腫瘍拒絶抗原 / MHC拘束性 / CD4^-CD8^-TCRαβ / 移植免疫 / T細胞 / CD4^-CD8^- / TCRのβ |
|---|
| Research Abstract |
Generation of in vitro CD4^-CD8^-TCR alphabeta CTL response against allogeneic MHC class I antigen and MHC class I-restricted antigen was investigated. We demonstrated that in mice that were depleted of CD8^+ cells, CD4^-CD8^-TCR alphabeta CTL were induced against allogeneic MHC class I antigen following activation of CD4^+ cells. On the other hand, against MHC-class I restricted antigen, CD8-depleted mice were incapable of generating CTL response. However, when target cells were MHC class II (and I) antigen positive cells, CTL with both CD4^+ and CD4^-CD8^-TCR alphabeta phenotypes were generated in CD8-depleted B6 mice. Thus, in this case, stimulation of CD4^+ T cells by MHC class II restricted antigen leads to generation of CD4^-CD8^-TCR alphabeta CTL specific for MHC class I restricted antigen. Moreover, CD4^-CD8^-TCR alphabeta CTL are capable of mediating rejection responses in vivo.
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