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.
|ジャーナル||Japanese Journal of Cancer Research|
|出版ステータス||Published - 4月 1993|
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