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中文摘要
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可移植的淋巴瘤细胞,称为网状细胞肉瘤(RCS),来自 SJL小鼠诱导强增殖反应和淋巴因子产生 同基因的LYL+2-T细胞,但不存在于F1杂交鼠的T细胞中 SJL和表达I-E的菌株。来自骨的胸腺和淋巴结细胞 无应答者F1的骨髓嵌合体进入SJL应答和DO SJL T 细胞,反之,从SJL到F1嵌合体的T细胞没有反应。 已证实RCS细胞不表达外源I-E-α 链和抗I-AS的单抗完全阻断T细胞 RCS刺激。标记表面的双向凝胶电泳法 I-A显示正常SJL脾中缺少酸性A-α链或RCS细胞 细胞,但至少部分存在于内毒素诱导的B细胞母细胞。这个 关于电荷而不是大小的分子不均一性通过 神经氨酸酶治疗,衣霉素治疗RCS和SJL 脾细胞I-A分子看起来是一样的。神经氨酸酶治疗 在衣霉素治疗取消的同时,增强RCS的能力 刺激同基因T细胞。新近获得的RCS特异性T细胞克隆 对RCS细胞和内毒素诱导的B细胞都有反应,但对 SJL或(SJL×BALB/c)F1代的静息脾细胞 同种异体(H_2B)B细胞。迄今为止的结果表明,T 受RCS刺激的细胞,其反应似乎需要 RCS在体内的生长,可能是激活的B细胞抗原的特异性 糖基化的I-A分子。这些T细胞可能在生理上代表 重要的自身反应性辅助细胞,在SJL小鼠中,它们被解除调控并 促进B细胞系淋巴瘤的生长。(磅)
英文摘要
Transplantable lymphoma cells, called reticulum cell sarcomas (RCS), from SJL mice induce strong proliferative responses and lymphokine production in syngeneic Lyl+ 2- T cells but not in T cells from F1 hybrid mice of SJL with strains expressing I-E. Thymus and lymph node cells from bone marrow chimeras of nonresponder F1 into SJL respond as well as do SJL T cells and, conversely, T cells from SJL to F1 chimeras fail to respond. It has been established that RCS cells do not express alien I-E-alpha chains, and monoclonal antibody to I-AS completely blocks T cell stimulation by RCS. Two-dimensional gel electrophoresis of labeled surface I-A show acidic A-alpha chains or RCS cells absent from normal SJL spleen cells but at least partially present on LPS-induced B-cell blasts. The molecular heterogeneity with respect to charge but not size is removed by treatment with neuraminidase, whereas tunicamycin-treated RCS and SJL spleen cell I-A molecules appear identical. Neuraminidase treatment enhances, while tunicamycin treatment abolishes, the ability of RCS to stimulate syngeneic T cells. Recently derived RCS-specific T cell clones respond to both RCS cells and to LPS-induced B cell blasts, but not to resting spleen cells from SJL or (SJL x BALB/c) F1 hybrids and not to allogeneic (H2b) B cell blasts. The results to date suggest that the T cells which are stimulated by RCS, and whose response appears needed for RCS growth in vivo, are specific for activated B cell antigens, possibly glycosylated I-A molecules. These T cells may represent physiologically important autoreactive helper cells which, in SJL mice, are deregulated and promote growth of lymphomas of the B cell lineage. (LB)
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HOST TUMOR INTERACTION IN BURKITTS LYMPHOMA
  • 批准号:
    2292081
  • 项目类别:
  • 资助金额:
    $3.28万
  • 财政年份:
    1994
  • 负责人:
    G. J THORBECKE
  • 依托单位:
HOST TUMOR INTERACTION IN BURKITTS LYMPHOMA
  • 批准号:
    2292080
  • 项目类别:
  • 资助金额:
    $3.0万
  • 财政年份:
    1994
  • 负责人:
    G. J THORBECKE
  • 依托单位:
GERIATRIC RESEARCH INSTITUTIONAL TRAINING (GRIT) AWARD
  • 批准号:
    3530563
  • 项目类别:
  • 资助金额:
    $12.55万
  • 财政年份:
    1991
  • 负责人:
    G. J THORBECKE
  • 依托单位:
GERIATRIC RESEARCH INSTITUTIONAL TRAINING (GRIT) AWARD
  • 批准号:
    3530565
  • 项目类别:
  • 资助金额:
    $12.9万
  • 财政年份:
    1991
  • 负责人:
    G. J THORBECKE
  • 依托单位:
海外基金