2002 Fiscal Year Final Research Report Summary
The roles of cytokines on the development of rheumatoid arthritis
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 |
Section | 一般 |
Research Field |
Immunology
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Research Institution | The University of Tokyo |
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)
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Project Period (FY) |
2000 – 2002
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Keywords | Rheumatoid Arthritis / Animal Models1 / IL-1 / HTLV-I / IL-6 / TNF-α / IL-17 / IL-1R antagonist |
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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Research Products
(13 results)
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[Publications] Nakae, S., Komiyama, Y., Narumi, S., Sudo, K., Horai, R., Tagawa, Y., Sekikawa, K., Matsushima, K., Asano, M., and Iwakura. Y.: "IL-1-induced TNFα elicits inflammatory cell infiltration in the skin by inducing interferon-γ-inducible protein-10 in the elicitation phase of contact hypersensitivity response"Int. Immunol.. 15. 251-260 (2002)
Description
「研究成果報告書概要(欧文)」より
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[Publications] Nakae, S., Komiyama, K., Yokoyama, H., Nambu, A., Umeda, M., Iwase, M., Homma, I., Sudo, K., Horai, R., Asano, M. and Iwakura. Y.: "Interleukin-1 is required for allergen-specific Th2 cell activation and the development of airway hypersensitivity response"Int. Immunol.. 15. 483-490 (2002)
Description
「研究成果報告書概要(欧文)」より
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[Publications] Nakae, S., Komiyama, Y., Nambu, A., Sudo, K., Iwase, M., Homma, I., Sekikawa, K., Asano, M., and Iwakura, Y.: "Antigen-specific T cell sensitization is impaired in IL-17-deficient mice, resulting in the suppression of allergic cellular and humoral responses"Immunity. 17. 375-387 (2002)
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「研究成果報告書概要(欧文)」より
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[Publications] Nakae, S., Saijo, S., Horai, R., Sudo, K., Mori, S., and Iwakura, Y.: "IL-17 production from activated T cells is required for the spontaneous development of destructive arthritis in mice deficient in IL-1 receptor antagonist"Proc. Natl. Acad. Sci. USA. 100. 5986-5990 (2002)
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「研究成果報告書概要(欧文)」より
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