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T cell antigen receptor and chain genes and MHC restriction

T cell antigen receptor and chain genes and MHC restriction
T细胞抗原受体和链基因以及MHC限制
批准号:
61570235
负责人:
YANAGI Yusuke
金额:
$1.41万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for General Scientific Research (C)
财政年份:
1986
资助国家:
日本
项目状态:
已结题
起止时间:
1986 至 1987

项目摘要

项目成果

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中文摘要
翻译
1. T细胞受体(TcR)由<alpha>和<beta>链组成。通过转移克隆基因和<beta>链基因,确定了这种<alpha><beta>异源二聚体负责T细胞的双重特异性。为了确定重要的氨基酸残基,我们从I-A^K反应性T细胞克隆MS 202中获得了具有改变的特异性的突变T细胞克隆。一个突变克隆E-3显示出对I-A^D和I-A^d以及I-A^K有反应。这种特异性变化似乎是由于E-o中TcR的结构变化所致,因为E-3中TcR的分子量小于MS 202。然而,TcR和链基因的核苷酸序列<alpha><beta>在MS 202和E-3之间是相同的。发现E-3在糖基化方面存在缺陷。此外,这两个克隆可能表达两种不同链的TcR分子。我们正在确定E-3.2特异性变化的原因。所有的小鼠抑制性T细胞克隆检查显示表达TcR<alpha>和<beta>链基因。我们目前正在利用消减杂交技术克隆抑制性T细胞中特异表达的基因.无论<alpha><beta>T细胞是否被抗原激活,编码TcR和TcR链的mRNA的量几乎不变. NZW<beta>小鼠的TcR链基因可能与(NZB × NZW)F_1小鼠的自身免疫有关。
英文摘要
1. The T cell receptor (TcR) is composed of <alpha> and <beta> chains. By transferring cloned and <beta> chain genes, it was established that this <alpha><beta> heterodimer is responsible for the dual specificity of T cells. However, it is still not known which amino acid residues are important in determining T cell specificities.In order to define important amino acid residues, we derived mutant T cell clones with altered specificities from an I-A^K reactive T cell clone, MS202. One mutant clone, E-3, was shown to respond to I-A^D and I-A^d as well as I-A^K. It seemed that this specificity change was due to the structural change of TcR in E-o as molecular weight of TcR was smaller in E-3 than in MS202. However, nucleotide sequences of TcR <alpha> and <beta> chain genes were identical between MS202 and E-3. It was found that E-3 has a defect in glycosylation. In addition, these two clones might express two kinds of TcR molecules with different chains. We are in a process of determining the cause of specificity change in E-3.2. All murine suppressor T cell clones examined were shown to express TcR <alpha> and <beta> chain genes. We are now in a process of cloning genes specifically expressed in suppressor T cells using the subtraction hybridization.3. The amount of mRNA coding for TcR <alpha> and <beta> chains was found to be almost constant whether T cells are activated by antigens or not.4. The TcR <beta> chain gene of NZW mice seems to contribute to the autoimmunity in (NZB x NZW)F_1 mice.
期刊论文(5)
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会议论文
柳雄介: Medical Immunology. 12. 302-303 (1986)
柳佑介:医学免疫学。12. 302-303 (1986)
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通讯作者:
Yanagi,Y.: "New Horizons in Animal Models for Autoimmune Disease.(T cell receptor gene deletion and autoimmunity in(NZB×NZW)【F_1】 mice)" Academic Press, (1987)
Yanagi, Y.:“自身免疫性疾病动物模型的新视野。((NZB×NZW)【F_1】小鼠中的T细胞受体基因缺失和自身免疫)”学术出版社,(1987)
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通讯作者:
Yanagi,Yusuke: "New Horizons in Animal Models for Autoimmune Disease:T cell receptor gene deletion and autoimmunity in (NZB×NZW)F_1 mice." Academic Press,Tokyo, 115-120 (1987)
Yanagi, Yusuke:“自身免疫性疾病动物模型的新视野:(NZB×NZW)F_1 小鼠中的 T 细胞受体基因缺失和自身免疫,东京学术出版社,115-120 (1987)”
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通讯作者:
Yanagi,Yusuke: "The T-cell antigen receptor and T-cell antigen recognition." Seikagaku. 60. 75-88 (1988)
Yanagi,Yusuke:“T 细胞抗原受体和 T 细胞抗原识别。”
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Mechanism of measles virus spread in the brain
Development of new therapy for congenital metabolic disorders using functional three-dimensional liver structures constructed by stem cells from human exfoliated deciduous teeth
  • 批准号:
    24592696
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 资助金额:
    $3.08万
  • 财政年份:
    2012
  • 负责人:
    YANAGI Yusuke
  • 依托单位:
Measles pathogenesis as studied using animal models
  • 批准号:
    21249032
  • 项目类别:
    Grant-in-Aid for Scientific Research (A)
  • 资助金额:
    $29.62万
  • 财政年份:
    2009
  • 负责人:
    YANAGI Yusuke
  • 依托单位:
Analysis of measles pathogenesis using the mouse model expressing measles virus receptor SLAM and recombinant viruses
  • 批准号:
    17209016
  • 项目类别:
    Grant-in-Aid for Scientific Research (A)
  • 资助金额:
    $32.45万
  • 财政年份:
    2005
  • 负责人:
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  • 依托单位:
海外基金