| Project/Area Number |
14570609
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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 |
Neurology
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| Research Institution | Nagasaki University |
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Principal Investigator |
NAKAMURA Tatsufumi Nagasaki University, Graduate School of Biomedical Sciences, Associate Professor, 大学院・医歯薬学総合研究科, 助教授 (00198219)
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| Co-Investigator(Kenkyū-buntansha) |
EGUCHI Katumi Nagasaki University, Graduate School of Biomedical Sciences, Professor, 大学院・医歯薬学総合研究科, 教授 (30128160)
SHIRABE Susumu Nagasaki University, Graduate School of Biomedical Sciences, Associate Professor, 大学院・医歯薬学総合研究科, 助教授 (40264220)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2003: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2002: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Natural killer (NK) cells / viral infection / HTLV-1 / apoptosis / HAM / 細胞傷害活性 / CD160分子 / PI-9分子 / NK / activation marker / PI-9 / Granzyme B |
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| Research Abstract |
Natural killer (NK) cell plays a pivotal role in eliminating virus-infected cells. However, viruses have learned how to manipulate host immune systems so that they can coexist with their host. In this paper, we focused on human T cell leukemia virus type I (HTLV-I) and examined how the virus prevents the elimination of host NK cells. Three strategies have been identified by which the virus ways evades NK cells :1) Virus downregulates CD 160 expression on NK cells leading to lack of NK cell cytotoxicity, 2)Virus induces NK cell death via CD58-CD2 interactions and/or cytokines stimulation (ie. IL-12); 3) Virus upregulates serpin proteinase inhibitor 9 (PI-9) in virus-infected cells, resulting in protection from granzyme B -mediated cell death.
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