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目的 :研究体内应用大鼠DC单抗WZD3对大鼠免疫状态的影响 ,在此基础上应用DC单抗同时处理供、受体 ,进行同种异体心脏移植 ,研究单抗诱导供、受体间双向移植耐受可能机理 ,为联合应用单抗和耐受性DC诱导移植免疫耐受奠定基础。方法 :用不同剂量WZD3处理SD(受体 )和Wistar(供体 )大鼠 ,两周后观察单向、双向混合淋巴细胞培养结果和经ConA或LPS刺激脾细胞产生的细胞因子水平变化。选择合适WZD3剂量同时对供、受体大鼠体内注射 ,进行异体异位心肺联合移植 ,术后观察移植器官存活时间和器官排斥终点时受体脾细胞分泌细胞因子水平。结果 :高剂量 (8mg kg体重 )WZD3对大鼠单向、双向MLC以及脾细胞产生IL 2和TNF有明显抑制作用 ,且能明显延长移植心脏存活时间 ;中剂量 (4mg kg体重 )和低剂量 (2mg kg体重 )WZD3对上述指标有轻度或无抑制作用。结论 :采用高剂量WZD3能下调大鼠免疫功能 ;同时处理供、受体大鼠 ,能诱导供、受体间双向免疫耐受 ,明显延长移植器官存活时间 ,其机制可能与清除DC、下调Th1细胞功能有关。
OBJECTIVE: To study the effect of rat monoclonal antibody (DC) monoclonal antibody (WZD3) on immune status in vivo and to study the effect of monoclonal antibody (DC) on the immune status of rats. The mechanism of bi-directional transplantation tolerance may lay the foundation for the combination of monoclonal antibody and tolerance DC induced immune tolerance of transplantation. Methods: SD (recipient) and Wistar (donor) rats were treated with different doses of WZD3. Two weeks later, the results of unidirectional and bidirectional mixed lymphocyte culture and the changes of cytokines produced by spleen cells stimulated by ConA or LPS were observed. Select the appropriate dose of WZD3 at the same time for donor and recipient rats in vivo injection of allogeneic cardiopulmonary transplantation, postoperative graft survival time and organ rejection end of the recipient spleen cells to secrete cytokines. Results: WZD3 at high dose (8 mg kg body weight) significantly inhibited IL 2 and TNF production in unidirectional and bidirectional MLC and spleen cells, and significantly prolonged cardiac allograft survival time. Middle dose (4 mg kg body weight) and low dose (2mg kg body weight) WZD3 mild or no inhibitory effect on the above indicators. Conclusion: WZD3 can down-regulate the immunological function of rats. Simultaneous treatment of donor and recipient rats can induce bidirectional immunotolerance between donors and recipients and significantly prolong the survival time of transplanted organs. The mechanism may be related to the clearance of DC and down-regulation of Th1 Cell function related.