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Role of Valpha24JalphaQ TCR T Cells in the Pathogenesis of Asthma

Role of Valpha24JalphaQ TCR T Cells in the Pathogenesis of Asthma
Valpha24JalphaQ TCR T 细胞在哮喘发病机制中的作用
批准号:
09670600
负责人:
IWAMOTO Itsuo
金额:
$2.18万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
1997
资助国家:
日本
项目状态:
已结题
起止时间:
1997 至 1998

项目摘要

项目成果

IWAMOTO Itsuo的其他基金

相关文献

中文摘要
翻译
特应性疾病是由产生IL-4和IL-5的辅助性T细胞2(Th 2)的激活失调引起的。因为IL-4的存在有效地增强幼稚T细胞向Th 2细胞的分化,所以寻找为幼稚T细胞提供IL- 4的细胞群是重要的。最近,一个独特的T细胞亚群,自然杀伤(NK)T细胞,已被证明产生大量的IL-4激活后,这表明它们在启动Th 2细胞分化的调节作用。为了确定NK T细胞是否在人类Th 2疾病中发挥作用,我们分析了哮喘和特应性皮炎(AD)患者的NK T细胞。我们对不变的Valpha 24 JalphaQ CD 4 ^-CD 8 ^- T细胞(可能是人类NK T细胞)进行了频率分析,发现哮喘和AD患者的NK T细胞显著减少。此外,我们发现来自健康受试者的大多数人类NK T细胞在活化时产生IFN-γ,但不产生IL-4。总之,这些结果表明,产生IFN-γ的NK T细胞的减少可能参与了特应性疾病如哮喘和AD的发病机制。
英文摘要
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.
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会议论文
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)
Sakamoto A 等人:“来自正常受试者的 TCR Vα24JαQ T 细胞(鼠类 NKI+T 细胞的人类对应物)的特征”J. Allergy Clin 102(出版中)。
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通讯作者:
Nakao A,et al.: "High-dose oral tolerance prevents antigeninduced eosinophil recruitment into the mouse airways." Int.Immunol.10. 387-394 (1998)
Nakao A 等人:“高剂量口服耐受可防止抗原诱导的嗜酸性粒细胞募集到小鼠气道中。”
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通讯作者:
Nakao A, et al: "High-dose oral tolerance prevents antigen-induced eosinophil recruitment into the mouse airways" Int.Immunol.10. 387-394 (1998)
Nakao A 等人:“高剂量口服耐受可防止抗原诱导的嗜酸性粒细胞募集到小鼠气道中”Int.Immunol.10。
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发表时间:
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影响因子: --
作者: []
通讯作者:
Nakao A,et al.: "High-dose oral tolerance prevents antigen-induced eosinophil recruitment into the mouse airways" Int.Immunol.10. 387-394 (1998)
Nakao A 等人:“高剂量口服耐受可防止抗原诱导的嗜酸性粒细胞募集到小鼠气道中”Int.Immunol.10。
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通讯作者:
Role of IL/25 in the regulation of allergic airway inflammation
  • 批准号:
    15590797
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 资助金额:
    $2.24万
  • 财政年份:
    2003
  • 负责人:
    IWAMOTO Itsuo
  • 依托单位:
Molecular Mechanism underlying Eosinophil Differentiation in Bronchial Asthma
  • 批准号:
    13670591
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 资助金额:
    $2.56万
  • 财政年份:
    2001
  • 负责人:
    IWAMOTO Itsuo
  • 依托单位:
Identification and characterization of activated genes of eosinophils in asthma
  • 批准号:
    11670566
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 资助金额:
    $2.11万
  • 财政年份:
    1999
  • 负责人:
    IWAMOTO Itsuo
  • 依托单位:
Mechanism of T cell activation in the airways of asthma
  • 批准号:
    07670659
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 资助金额:
    $1.54万
  • 财政年份:
    1995
  • 负责人:
    IWAMOTO Itsuo
  • 依托单位: