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2002 Fiscal Year Final Research Report Summary

The roles of cytokines on the development of rheumatoid arthritis

Research Project

Project/Area Number 12470076
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Research Field Immunology
Research InstitutionThe University of Tokyo

Principal Investigator

IWAKURA Yoichiro  Instittute of Medical Science, Professor, 医科学研究所, 教授 (10089120)

Co-Investigator(Kenkyū-buntansha) SUDO Katsuko  Institute of Medical Science, Research Associate, 医科学研究所, 助手 (50126091)
Project Period (FY) 2000 – 2002
KeywordsRheumatoid 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.

  • Research Products

    (13 results)

All Other

All Publications (13 results)

  • [Publications] Nakae, S.: "IL-1-induced TNE elicits inflammatory cell infiltration in the skin by inducing interferon-g-inducible protein-10 in the elicitation phase of CHS"Int. Immunol.. 15. 251-260 (2003)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Nakae, S.: "Interleukin-1 is required for allergen-specific Th2 cell activation and the development of airway hypersensitivity response"Int. Immunol.. 15. 483-490 (2003)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Nakae, S.: "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)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Nakae, S.: "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. USA. 100. 5986-5990 (2003)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Iwakura, Y.: "Roles of IL-1 in the development of rheumatoid arthritis : Consideration from mouse models"Cytokine Growth Factor Rev.. 13. 341-355 (2002)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Saijo, S.: "Suppression of autoimmune arthritis in IL-1-deficient mice in which T cell activation is impaired due to low levels of CD40L and OX40 expression on T cell"Arth. Rheum.. 13. 533-544 (2002)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Iwakura, Y.: "Autoimmune chronic inflammatory arthropathy in mice transgenic for the HTLV-I tax gene"Gann Monograph. (in press). (2003)

    • Description
      「研究成果報告書概要(和文)」より
  • [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
  • [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
  • [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)

    • Description
      「研究成果報告書概要(欧文)」より
  • [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)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Iwakura, Y.: "Roles of IL-1 in the development of rheumatoid arthritis : Consideration from mouse models"Cytokine Growth Factor Rev.. 13. 341-355 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Saijo, S., Asano, M., Horai, R., Yamamoto, H., and Iwakura. Y.: "Suppression of autoimmune arthritis in IL-1-deficient mice in which T cell activation is impaired due to low levels of CD40L and OX40 expression on T cells"Arth. Rheum.. 46. 533-544 (2002)

    • Description
      「研究成果報告書概要(欧文)」より

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Published: 2004-04-14  

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