PROPERTIES OF LYMPHOID TUMOR CELLS IN VIVO-IN VITRO

可移植的淋巴瘤细胞，称为网状细胞肉瘤（RCS）， SJL小鼠诱导强烈的增殖反应和淋巴因子产生， 同源赖氨酸+ 2- T细胞，而不是在T细胞从F1 杂交小鼠 SJL与表达I-E的菌株。 来自骨的胸腺和淋巴结细胞 无应答者骨髓嵌合体1 进入SJL响应以及进行SJL T 细胞，相反，T细胞从SJL到F1 嵌合体没有反应 已经确定RCS细胞不表达外来I-E-alpha 链和抗I-A的单克隆抗体S 完全阻断T细胞 RCS的刺激。 标记表面的双向凝胶电泳 I-A显示正常SJL脾中不存在酸性A-α链或RCS细胞 细胞，但至少部分存在于LPS诱导的B细胞母细胞上。 的 关于电荷而不是尺寸的分子异质性被去除， 用神经氨酸酶治疗，而衣霉素治疗的RCS和SJL 脾细胞I-A分子看起来相同。 神经氨酸酶处理 增强，而衣霉素处理废除，RCS的能力， 刺激同基因T细胞。 最近衍生的RCS特异性T细胞克隆 对RCS细胞和LPS诱导的B细胞母细胞都有反应，但对 来自SJL或（SJL x BALB/c）F的静息脾细胞1 杂交种，而不是 同种异体（H2B）B细胞母细胞。 迄今为止的结果表明，T 受RCS刺激的细胞，其响应似乎需要 RCS在体内的生长，对活化的B细胞抗原具有特异性，可能 糖基化的I-A分子。 这些T细胞在生理上可能代表 在SJL小鼠中，重要的自身反应性辅助细胞被失调， 促进B细胞谱系淋巴瘤的生长。 （LB）

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)