| Project/Area Number |
07671736
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Urology
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| Research Institution | Nagasaki Univeristy |
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Principal Investigator |
KOGA Shigehiko NAGASAKI UNIV., SCHOOL OF MED., HOSPITAL LECTURER, 医学部・附属病院, 講師 (10205354)
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| Co-Investigator(Kenkyū-buntansha) |
KANETAKE Hiroshi NAGASAKI UNIV., SCHOOL OF MED., ASSISTANT PROFEDDOR, 医学部, 助教授 (50100839)
SAITO Yutaka NAGASAKI UNIV., SCHOOL OF MED., PROFESSOR, 医学部, 教授 (70039832)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1996: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1995: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | graft rejection / immune tolerance / nitric oxide |
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| Research Abstract |
The mechanisms by which immune competent cells mediate allograft injury tissue is still controversial. Many experiments support the view the allosensitized cytotoxic T cells (CTL) and non-specific inflammatory mediators play a crititcal role in graft rejection.
We demonstrated that DST prevented the development of CTL activity in the sponge matrix allograft as demonstrated by both direct in vitro cytotoxicity assays and limiting dilution analysis of graft infiltrating cells. DST was also associated with depressed NO synthesis by enhanced PGE2 production in the murine sponge allograft model.
Tacrolimus suppressed the CTL activity and NO production. However, NO production of graft infiltrating cells increased after restimulation with IFNgamma/LPS.Allogeneic DTH was suppressed by NOS inhibitor.
NO was related with immunoregulatory effects both in vitro and in vivo significantly. NO may be also effective as a marker of immune activation.
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