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Role of Valpha24JalphaQ TCR T Cells in the Pathogenesis of Asthma

Research Project

Project/Area Number 09670600
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Respiratory organ internal medicine
Research InstitutionChiba University Scool of Medicine

Principal Investigator

IWAMOTO Itsuo  Chiba University, Associate Professor, 医学部, 助教授 (10111436)

Co-Investigator(Kenkyū-buntansha) KURASAWA Kazuhiro  Chiba University, Assistant, 医学部, 助手 (30282479)
Project Period (FY) 1997 – 1998
Project Status Completed (Fiscal Year 1998)
Budget Amount *help
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 1998: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1997: ¥2,200,000 (Direct Cost: ¥2,200,000)
KeywordsAsthma / Valpha24JalphaQ TCR / NK T cells / IFN-gamma / Th2 cells / Th2タイプ免疫応答 / TCR / 免疫制御
Research Abstract

Atopic disorders are caused by disregulated activation of T helper 2 (Th2) cells that produce IL-4 and IL-5, Because the presence of IL-4 potently augments the differentiation of naive T cells into Th2 cells, it is important to seek the cell population which provides IL- 4 for naive T cells. Recently, a unique subpopulation of T cells, natural killer (NK) T cells, has been shown to produce a large amount of IL-4 upon activation, suggesting their regulatory role in initiation of Th2 cell differentiation. To determine whether NK T cells play a role in human Th2 diseases, we analyzed the NK T cells in patients with asthma and atopic dermatitis (AD). We performed a frequency analysis of the invariant Valpha24JalphaQ CD4^-CD8^- T cells, probable human NK T cells, and found that the NK T cells are significantly decreased in patients with asthma and AD.In addition, we found that the majority of human NK T cells from healthy subjects produce IFN-gamma but not IL-4 upon activation. Taken together, these results suggest that the decrease of NK T cells, which produce IFN-y, may be involved in the pathogenesis of atopic diseases, such as asthma and AD.

Report

(3 results)
  • 1998 Annual Research Report   Final Research Report Summary
  • 1997 Annual Research Report
  • Research Products

    (6 results)

All Other

All Publications (6 results)

  • [Publications] Nakao A, et al: "High-dose oral tolerance prevents antigen-induced eosinophil recruitment into the mouse airways" Int.Immunol.10. 387-394 (1998)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1998 Final Research Report Summary
  • [Publications] Sano H, et al: "Cross-linking of ICAM-1 induces interleukin-8 and RANTES production through the activation of MAP kinases" biochem. Biophys. Res. Commun.250. 694-698 (1998)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1998 Final Research Report Summary
  • [Publications] Nakao A,et al.: "High-dose oral tolerance prevents antigeninduced eosinophil recruitment into the mouse airways." Int.Immunol.10. 387-394 (1998)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1998 Final Research Report Summary
  • [Publications] Nakao A,et al.: "High-dose oral tolerance prevents antigen-induced eosinophil recruitment into the mouse airways" Int.Immunol.10. 387-394 (1998)

    • Related Report
      1998 Annual Research Report
  • [Publications] Sano H,et al.: "Cross-linking of ICAM-1 induces interleukin-8 and RANTES production through the activation of MAP kinases." Biochem.Biophys.Res.Commun.250. 694-698 (1998)

    • Related Report
      1998 Annual Research Report
  • [Publications] Sakamoto A, et al: "Charactaristics of TCR Vα24JαQ T cells,a human counterpart for murine NKI^+ T cells, from normal subjects" J.Allergy Clin.Immunol. 102(印刷中). (1998)

    • Related Report
      1997 Annual Research Report

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Published: 1997-04-01   Modified: 2016-04-21  

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