中文摘要：

许多癌症治疗的功效由于他们导致 apoptosis 的能力。DR5 能与它的自然 ligand 在绑定以后激活 apoptosis 小径，瘤坏死因素相关的导致 apoptosis ligand (TRAIL/Apo2L ) 。小道和论战的 anti-DR5 monoclonal 抗体当前为癌症治疗正在被探索。我们对 DR5 的以前准备的 monoclonal 抗体 A6 的 cytotoxicity 的机制这里被调查。A6 能在能被归因于 apoptosis 小径的激活的时间依赖者和剂量依赖者举止引起生存能力 Jurkat 房间的损失。Caspases 3， 8 和 9 在 Jurkat 房间和 caspase 被激活特定的禁止者例如宽广 caspases 禁止者 Z-VAD-FMK， caspase 9 特定的禁止者 Z-LEHD-FMK 能恢复的 8 特定的禁止者 Z-IETD-FMK 和 caspase 生存能力损失由 A6 引起了。功能和调停小道的 apoptosis 的分子的机制也被调查并且与那些相比 A6。尽管 A6 和小道认出不同 epitope，他们能在 Jurkat 房间导致类似的反应。

英文摘要：

The efficacy of many cancer treatments is due to their ability to induce apoptosis. DR5 can activate apoptosis pathway after binding with its natural ligand, tumour necrosis factor-related apoptosis-inducing ligand （TRAIL/ Apo2L）. Both TRAIL and agonistic anti-DR5 monoclonal antibody are currently being explored for cancer therapy. The mechanisms of cytotoxicity of our previously prepared monoclonal antibody A6 against DR5 were investigated here. A6 could cause viability loss of Jurkat cells in both time- and dose-dependent manner which could be attributed to the activation of apoptosis pathway. Caspases 3, 8 and 9 were activated in Jurkat cells and the caspase specific inhibitors, such as broad caspases inhibitor Z-VAD-FMK, caspase 8 specific inhibitor Z-IETDFMK and caspase 9 specific inhibitor Z-LEHD-FMK could recover the viability loss caused by A6. The function and molecular mechanism of TRAIL-mediated apoptosis were also investigated and compared with those of A6. Although A6 and TRAIL recognize a different epitope, they could induce a similar reaction in Jurkat cells.