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Effect of Accessory Cells on Stimulation of Murine T‐CellLeukemia with Antibodies to the CD3/T Cell Antigen Receptor Complex

机译:辅助细胞对小鼠T细胞刺激的影响白血病的CD3 / T细胞抗原受体复合物抗体

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摘要

Stimulation of EL4 and RL1 leukemia cells in vitro with immobilized anti‐CD3ε monoclonal antibody (mAb) (145–2C11) or anti‐TCRβ mAb (H57–597) in the absence of accessory cells induced interleukin‐2 (IL‐2) production, and caused growth inhibition. The growth inhibition was, however, transient and the tumors started to grow again within 5 days in immobilizing plates treated with antibodies at concentrations of 2.5–100 μg/ml. Addition of mitomycin C‐treated accessory cells to the culture inhibited IL‐2 production and resulted in augmented and persistent growth inhibition. No recovery of tumor growth was observed. Furthermore, DNA from EL4 and RL1 leukemia cells stimulated with anti‐CD3/TCR mAbs was fragmented even in the absence of accessory cells, but fragmentation was much greater in the presence of accessory cells. Marginal and high expression of the bcl‐2 gene were observed in EL4 and RL1, respectively, indicating that apoptosis of these leukemias mediated by signalling through the CD3/TCR complex has no direct relationship with expression of the bcl‐2 gene.
机译:在不存在辅助细胞的情况下,用固定的抗CD3ε单克隆抗体(mAb)(145-2C11)或抗TCRβmAb(H57-597)刺激EL4和RL1白血病细胞的体外诱导白介素-2(IL-2)的产生,并引起生长抑制。然而,生长抑制是短暂的,并且在固定化板中用2.5-100μg/ ml的抗体处理的肿瘤在5天内开始再次生长。将丝裂霉素C处理过的辅助细胞添加到培养物中会抑制IL-2的产生,并导致增强的持久性生长抑制作用。没有观察到肿瘤生长的恢复。此外,即使在不存在辅助细胞的情况下,用抗CD3 / TCR mAb刺激的EL4和RL1白血病细胞的DNA也会被片段化,但是在存在辅助细胞的情况下,片段化会更大。在EL4和RL1中分别观察到bcl-2基因的边缘和高表达,这表明通过CD3 / TCR复合物信号传导介导的这些白血病的凋亡与bcl-2基因的表达没有直接关系。

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