| Project/Area Number |
04454116
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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 |
基礎獣医学
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| Research Institution | University of Tokyo |
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Principal Investigator |
ONODERA Takashi The Univ.of Tokyo, Fac.of Agri.Professor, 農学部, 教授 (90012781)
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| Co-Investigator(Kenkyū-buntansha) |
YUKAWA Masayoshi Nihon Univ.Colleg of Agr., and Vet, Prof., 農獣医学部, 助教授 (50107249)
MATSUMOTO Yoshitsugu The Univ.of Tokyo, Fac.of Agri.Assoc.Prof., 農学部, 助教授 (00173922)
ONO Kenichiro The Univ.of Tokyo, Fac.of Agri.Professor, 農学部, 教授 (50111480)
DOI Kunio The Univ.of Tokyo, Fac.of Agri.Professor, 農学部, 教授 (70155612)
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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 |
¥6,300,000 (Direct Cost: ¥6,300,000)
Fiscal Year 1993: ¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 1992: ¥3,400,000 (Direct Cost: ¥3,400,000)
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| Keywords | interferon / pseudorabies virus / serum thymic factor / macrophage / NK cell / macrophage activity / anti-asialo GM1 / VSV / 1型糖尿病 |
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| Research Abstract |
Susceptibility to pseudorabies virus (PRV) infection in mice, which were continuously depleted of natural killer (NK) cell activity by injection of anti-asialo GM1, was examined. Effects of serum thymic factor (FTS) on susceptibility of mice to PRV were also investigated. In mice with depleted NK cell activity, the mortality of PRV-infected mice was markedly high, whereas that of FTS-pretreated mice was significantly lower than the controls. Reduced susceptibility to PRV was demonstrated in mice treated with anti-asialo GM1 antisera before the PRV infection. Such a reduced susceptibility was not observed in mice inoculated with the antisera on day 1 post-infection. To analyze the FTS-induced resistance to PRV infection, NK cell activity, macrophage activity, and interferon (IFN) productions were studied. Interferon production and NK cell activity were enhanced in the FTS-pretreated mice, suggesting that interferon may play an important role in this FTS-induced resistance to PRV infection.
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