CD4^+ CD25^+调节性T细胞在大鼠递增负荷过度训练中的表达及其免疫调节功能

Expression and Immunomodulatory Functions of CD4^+ CD25^+ T-cell in Progressively Increasing Load Overtraining in Rats

研究CD4+ CD25+调节性T细胞在大鼠递增负荷过度训练中的表达及其免疫调节功能。方法:对雌性SD大鼠进行9周递增负荷过度训练,分别在训练的第1周、第3周、第9周训练结束后的36 h,以及恢复1周后处死大鼠。ELISPOT法检测Th1/Th2型淋巴细胞亚群表达,同时采用流式细胞术对CD4+ CD25+调节性T细胞进行动态观察。结果:递增运动负荷训练过程中免疫机能结果表明,Th1型细胞因子IFN-γ在第1周跑台训练后升高;而第3周的跑台训练后,又表现为明显的抑制;恢复期1周后,实验组IFN-γ明显受到抑制。Th2型细胞因子IL-4最显著的变化发生在递增负荷训练结束后的恢复期(恢复1周),此时IL-4较对照组升高了1.44倍。CD4+ CD25+T细胞的表现:第1周的运动负荷后显著升高;第9周递增负荷训练结束后的恢复期,呈下降趋势。结论:中等强度运动后免疫机能的Th1漂移可能是运动诱发CD4+ CD25+T细胞增强,从而抑制Th2淋巴亚群分化所致。过度疲劳运动造成CD4+ CD25+T细胞的部分抑制,减弱了CD4+ CD25+T细胞选择性抑制Th2增殖和活化的功能,免疫机能向Th2方向漂移。

The present research aims to research the expression and immunomodulatory functions of CD4＋ CD25＋ T-cell in progressively increasing load overtraining in Rats.Method： Normal female Sprague-Dawly rats were trained with a progressively increasing load for nine weeks,and samples were collected at different times： at 36 h respectively after the 1st,3rd,9th week＇s training and also one week after recovery.After samples collected,Th1/Th2 immune balance was evaluated by ELISPOT,and CD4＋ CD25＋ T-cells were viewed dynamically using FCM.Results： Immune function changes： Th1 cytokine IFN-γ increased after the first week training,but decreased after 3rd week training.One week after the whole training session,IFN-γ in the training group sharply declined.The remarkable change in Th2 cytokine 1L-4 occurred in the recovery period after the training.IL-4 was 1.44 times higher than that in the control group.CD4＋ CD25＋T-cells increased obviously after the first week training,but were in a decreasing trend in the recovery stage after the nine weeks＇ training.Conclusions： The Th1 drift of immune functions after moderate activities may result from of enhancing of CD4＋ CD25＋T-cells caused by physical activities and hence restrained the polarization of Th2 subset.Excessive exercises partly suppressed CD4＋ CD25＋T-cells and reduced CD4＋ CD25＋T-cells＇ function in restraining the multiplication and activation of Th2,hence immune functions drifted toward Th2.