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作 者:叶俊生[1] 李娟[2] 周敏捷[1] 夏仁飞[1]
机构地区:[1]南方医科大学南方医院肾移植科,广东广州510515 [2]南方医科大学护理学院,广东广州510515
出 处:《医学临床研究》2016年第8期1470-1474,共5页Journal of Clinical Research
基 金:广东省自然科学基金(2016A030313566);南方医科大学南方医院院长基金(20152010);广东省医学科研基金(A2015241)
摘 要:[目的]探讨经体外光化学疗法(extracorporeal photopheresis,ECP)处理后的供者淋巴细胞预输注对小鼠心脏移植后移植物存活的影响。[方法]采用小鼠腹部异位心脏移植模型,供者为BALB/C小鼠,受者为C57BL/6小鼠。实验分为两组:对照组直接行心脏移植手术,ECP组于术前7d分离供者脾脏淋巴细胞,给予ECP处理后回输给受者,移植后观察移植物存活情况;部分受者于术后7d获取脾脏用于流式细胞术检测,移植心脏者行HE染色观察其组织学特点,并用免疫组化法检测组织T淋巴细胞浸润。[结果1ECP组移植心脏存活时间延长(20±4.67dVS7.5±0.70d,P〈0.001),伴有移植物排斥反应减轻,淋巴细胞浸润减少,以及外周效应性T细胞生成减少,CD4+CD25+goxp-3+调节性T细胞增加。[结论]供者淋巴细胞ECP处理后预输注能延长小鼠移植心脏存活时间,其机制可能在于ECP诱导的凋亡淋巴细胞预输注减少了效应性T细胞的数量,并且增加了调节性T细胞的产生。[Objective] To investigate the effects of extracorporeal photopheresis(ECP) treated donor lym- phocyte infusion on graft survival after murine heart transplantation. [Methods]Abdominal ectopic heart trans- plantations were performed using BALB/C mice as donors and C57BL/6 mice as recipients. Mice in the control group did not receive any treatment other than transplantation. For mice in ECP treated group, donor spleno- cytes suspension was treated by ECP and then injected into recipients via penis vein 7 days before transplanta- tion. The graft survival was assessed by abdominal palpation after transplantation. The spleen were harvested on day 7 for further flow cytometry test; and the H&E staining and immunohistochemistry staining of T lym- phocyte of graft tissue was evaluated. [Results]The graft survival time in the ECP treated group was signifi- cantly prolonged compared to the control group(20±4.67 d vs 7.5±0.70 d, P〈0.001). The frequency of ef- fective T cells in the spleens of recipients in ECP treated group was significantly decreased compared to in the spleens of recipients in the control group. The frequency of CD4+ CD25+ Foxp-3+ regulatory T cells in the spleen of ECP treated mice was higher than that of control group mice. [Conclusion]Infusion of ECP treated donor lymphocytes prolongs grab survival alter routine heart transplantation, possibly via suppressing effector T cell reaction and induction of regulatory T cell generation.
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