| Project/Area Number |
08457081
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
寄生虫学(含医用動物学)
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| Research Institution | Kyusyu University |
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Principal Investigator |
TADA Isao Kyusyu University Faculty of Medicine Professor, 医学部, 教授 (60064531)
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| Co-Investigator(Kenkyū-buntansha) |
KISHIHARA Kenji Kyusyu University Medical Insttitute of Bioregulation Research Associate, 生体防御研究所, 助手 (80214774)
KOGA Masataka Kyusyu University Faculty of Medicine Lecturer, 医学部, 講師 (80136449)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥4,400,000 (Direct Cost: ¥4,400,000)
Fiscal Year 1997: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1996: ¥3,700,000 (Direct Cost: ¥3,700,000)
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| Keywords | Strongyloides ratti / Knockout mouse / Mast cell / CD8+T cell / Expulsion / Protective immunity / Testosterone / Macrophage / CD8+T細胞 / 防御免疫 / 肥満細胞 / goblet cell |
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| Research Abstract |
In the fiscal years 1996 and 1997, aiming at the analysis of the mechanism concerned in the protective immunity against the infection of intestinal nematode, we studied Strongyloides ratti (Sr) infection in the CD45 exon 6-deficient mice (CD45-1-). Following results were obtained :
1) In CD45-/-, the protective immunity was markedly reduced and the period of infection lasted remarkably longer than the control.
2) Sr infection in CD45-/-inoculated with splenocytes revealed that the marked reduction of protective immunity does not depend only on the T cell dysfunction .
3) Induction of mucous mast cells (MMC) by the adiministration of IL-3 did not cause the expulsion in CD45-/- probably bacause of the dysfunction of MMC itself.
4) CD8+T cells were considered not essential in the protection against Sr in CD45-/-. The unique character of CD45-/- was shown in this study.
5) Influence of testosterone on the macrophage activity in the protection was investigated. The study revealed that testosterone promoted the protection inhibition when the macrophagaes were damaged by carbon.
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