• Search Research Projects
  • Search Researchers
  • How to Use
  1. Back to previous page

Functional analysis of the non-HLA genes within major histocompatibility complex (MHC) region with the use of gene-targeted mice

Research Project

Project/Area Number 13670320
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Immunology
Research InstitutionUniversity of Tokushima

Principal Investigator

MATSUMITO Mitsuru  Institute for Enzyme Research, Professor, 分子酵素学研究センター, 教授 (60221595)

Co-Investigator(Kenkyū-buntansha) MATSUSHIMA Akemi  Institute for Enzyme Research, Lecturer, 分子酵素学研究センター, 教務員 (70116862)
Project Period (FY) 2001 – 2002
Project Status Completed (Fiscal Year 2002)
Budget Amount *help
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2002: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2001: ¥1,800,000 (Direct Cost: ¥1,800,000)
KeywordsLymphotoxin receptor / Signal transduction / NF-Kb / NIK / T cell / リンホトキシン / TNFレセプター / ノックアウトマウス
Research Abstract

NF-Kb-inducting kinase (NIK) is involved in lymphoid organogenesis in mice through lymphotoxin-b receptor signaling. To clarify the roles of NIK in T cell activation through TCR/CD3 and co atimulation pahways, we have studied the function of T cells from aly mice, a strain with mutant NIK. NIK mutant T cells showed impaired proliferation and IL-2 production in respones to anti-CD3 stim ulation, and these effects were caused by impaired NF-Kb activity in both mature and immature T cells; the impaired NF-Kb. In contrast, responses to co- stimulatory signals were largely retained in aly mice, suggesting that NIK is not uniquely coupled to the co-stim ulatory pathways. When NIK mutant T cells were stimulated in the presence of a protein kinase C (PKC) inhibitor, proliferative responses were abrogated more severely than in control mice, suggesting that both NIK and PKC control T cell activation in a cooperative manner. We also demonstrated that NIK and PKC are involved in distinct NF-Kb activation pathways downstream of TCR/CD3. These results suggest critical roles for NIK in setting the threshold for T cell activation, and partly account for the immunodeficiency in aly mice.

Report

(3 results)
  • 2002 Annual Research Report   Final Research Report Summary
  • 2001 Annual Research Report
  • Research Products

    (6 results)

All Other

All Publications (6 results)

  • [Publications] Matsumoto, M., et al.: "Essential role of NF-κB-inducing kinase in T cell activation through the TCR/CD3 pathway"Journal of Immunology. 169. 1151-1158 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Matsushima, A., et al.: "Essential role of NF-κB-inducing kinase and IκB-kinase α in NF-κB activation through lymphotoxin-β receptor, but not through TNF receptor-I"Journal of Experimental Medicine. 193. 631-636 (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Matsumoto,M, et al.: "Essential role of NF-Kb-inducing kinase in T cell activation through the TCR/CD3 pathway"Journal of Immunology. 169. 1151-1158 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Matsushima,A, et al.: "Essential role of NF-Kb-inducing kinase and IkB-kinase a in NF-Kb activation through lymphotoxin-B receptor, but not through TNF receptor-I"Journal of Experimental Medicine. 193. 631-636 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Matsumoto, M., et al.: "Essential role of NF-κB-inducing kinase in T cell activation through the TCR/CD3 pathway"Journal of Immunology. 169. 1151-1158 (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] Matsushima, A., et al.: "Essential role of NF-κB-inducing kinase and IκB-kinase αin NF-κB activation through lymphotoxin-β receptor, but not through TNF receptor-I"Journal of Experimemtal Medicine. 193(5). 631-636 (2001)

    • Related Report
      2001 Annual Research Report

URL: 

Published: 2001-04-01   Modified: 2016-04-21  

Information User Guide FAQ News Terms of Use Attribution of KAKENHI

Powered by NII kakenhi