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目的:验证在小鼠心脏移植中,2,3,7,8-四氯二苯二氧芑(TCDD)激活芳香烃受体(AHR)是否可以诱导调节性T细胞(Treg)扩增以及减轻急性排斥反应。方法:建立小鼠心脏移植模型,给予TCDD,观察对排斥反应及移植物生存期的影响。体外实验评估TCDD对Treg细胞比例的影响。检测受者体内Treg细胞比例及白细胞介素(白介素)-10表达水平。结果:TCDD激活AHR明显减轻心脏移植物内急性排斥反应,延长移植物存活时间[MST=(23.5±7.7)d]。体外实验中TCDD明显提升CD4+CD25+Foxp3+调节性T细胞比例[TCDD组(15.3±2.6)%;PBS组(4.7±2.4)%,P<0.01)],而受者体内脾脏和移植物内Treg细胞比例相比对照组也明显升高(P<0.05)。同时,TCDD明显提升了受者体内白介素-10的表达水平。结论:术前单次给予TCDD激活AHR可以明显抑制小鼠同种心脏移植物急性排斥反应,其机制可能与扩增Treg亚群有关。
PURPOSE: To demonstrate whether 2,3,7,8-tetrachlorodibenzodioxine (TCDD) -activated aromatic hydrocarbon receptor (AHR) can induce the expansion and mitigation of regulatory T cells (Tregs) in cardiac allografts of mice Acute rejection. Methods: The mouse heart transplantation model was established and TCDD was given to observe the effects on rejection and graft survival. The effect of TCDD on Treg cell ratio was evaluated in vitro. The proportion of Treg cells and the expression of interleukin (IL-10) in recipients were detected. Results: Activation of AHR by TCDD significantly attenuated the acute rejection in heart grafts and prolonged graft survival [MST = (23.5 ± 7.7) d]. TCDD in vitro significantly increased the proportion of CD4 + CD25 + Foxp3 + regulatory T cells (15.3 ± 2.6% in TCDD group and 4.7 ± 2.4% in PBS group, P <0.01) Treg cell ratio was also significantly higher than the control group (P <0.05). At the same time, TCDD significantly enhances the expression of interleukin-10 in recipients. Conclusion: A single preoperative administration of TCDD activates AHR can significantly inhibit the acute rejection of allograft heart transplantation in mice. The mechanism may be related to the expansion of Treg subsets.