| Project/Area Number |
12470076
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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 |
Immunology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
IWAKURA Yoichiro Instittute of Medical Science, Professor, 医科学研究所, 教授 (10089120)
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| Co-Investigator(Kenkyū-buntansha) |
SUDO Katsuko Institute of Medical Science, Research Associate, 医科学研究所, 助手 (50126091)
宝来 玲子 東京大学, 医科学研究所, 助手 (20313091)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥14,100,000 (Direct Cost: ¥14,100,000)
Fiscal Year 2002: ¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 2001: ¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 2000: ¥6,100,000 (Direct Cost: ¥6,100,000)
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| Keywords | Rheumatoid Arthritis / Animal Models1 / IL-1 / HTLV-I / IL-6 / TNF-α / IL-17 / IL-1R antagonist / 自己免疫疾患 / トランスジェニックマウス / ノックアウトマウス / HTLV-1 |
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| Research Abstract |
We have produced transgenic mice carrying tax gene of HTLV-I (HTLV-I Tg) and IL-1 receptor antagonist knockout (IL-1Ra KO) mice, and found these mice spontaneously develop autoimmune arthritis. Also, we have reported that T cell dependent cellular immunity is crucial for the development of the disease. In this project, we evaluated that the roles of cytokine on the development of the autoimmune arthritis using those 2 mouse models. We showed that IL-1 and IL-6 is crucial for the development of the disease of HTLV-I Tg and TNF-a is required in the disease of IL-1Ra KO mice. Unlike other cytokines, IL-17 is known to be produced by the activated CD4 T cells, and induces other cytokines and chemokines. Also, it is suggested to be involved in rheumatoid arthritis in humans, because this cytokine is detected in the joints of the patients. Then, we produced IL-17 knockout (IL-17 KO) mice, and found that IL-17 deficiency completely suppresses the disease in the IL-1Ra KO mice.
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