| Project/Area Number |
01480172
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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 |
寄生虫学(含医用動物学）
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| Research Institution | TOKYO MEDICAL AND DENTAL UNIVERSITY |
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Principal Investigator |
FUJITA K Tokyo Medical and Dental University, Faculty of Medicine, Professor, 医学部, 教授 (90053107)
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| Co-Investigator(Kenkyū-buntansha) |
TSUKIDATE S Tokyo Medical and Dental University Faculty of Medicine, researcher, 医学部, 助手 (40121256)
YAMAOKA K Tokyo Medical and Dental University Faculty of Medicine, Lecturer, 医学部, 講師 (50220231)
YAMAMOTO K Tokyo Medical and Dental Univertisy Medical Research Institute, Professor, 難治疾患研究所, 教授 (40000971)
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| Project Period (FY) |
1989 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥7,400,000 (Direct Cost: ¥7,400,000)
Fiscal Year 1991: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1990: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1989: ¥5,500,000 (Direct Cost: ¥5,500,000)
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| Keywords | filaria / strogyloides / evasive mechanism / ATL-virus / CD^+8 t cell / IL-2 / IL-2 receptor / asialo GM_1^+ NK cell / asialo GM^+NK細胞 / ILー2R / マクロファ-ジ / 好酸球 / ミクロフィラリア / CD^<8+>細胞 / T細胞抑制 |
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| Research Abstract |
Seroepidemiological studies revealed that filarial as well as strongyloides parasites effected on infestation of adult T-cell leukemia (ATL) virus by our studies of the Goto Island, Nagasaki, Tomigusuku, Okinawa, Kikai Island, Kagoshima and Ashikita, Kumamoto. In this study, we succeeded in making clear the influence of these parasites on T cell, NK cell and/or lymphokines of the host, and also the effects of these parasites on the infestation of ATL virus in cell level.
It was shown in the first report that strongyloides infection elevated the ATL antibody titer of the infected host, but the clevation of the infestation of ATL virus within cell line was not observed in our experiments.
On the other hands, it was reported in our study that the filarial infection suppressed the immune response of the host non-specifically by CD+8 T cells, decreased the number of IL-2 receptor as well as IL-2 itself, and also decreased the function of NK cell.
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