CD4^+CD25^+T细胞在实验性重症肌无力中的作用研究  

MECHANISM OF PERIPHERAL IMMUNOTOLERANCE DISORDER IN EAMG MICE

作　　者：李劲频[1] 刘竞丽[1] 莫雪安[1] 孙圣刚[2] 

机构地区：[1]广西医科大学第一附属医院神经内科,南宁530021 [2]华中科技大学同济医学院附属协和医院神经内科,武汉430022

出　　处：《广西医科大学学报》2012年第3期342-344,共3页Journal of Guangxi Medical University

基　　金：广西科学基金资助项目(No.桂科青0728071)

摘　　要：目的:探讨实验性自身免疫性重症肌无力(EAMG)模型小鼠外周免疫耐受机制异常在疾病发生、发展中的作用。方法:检测成模组小鼠CD4+脾细胞中CD4+CD25+T细胞(Treg)水平,脾细胞Foxp3mRNA的表达情况,并与未成模组、弗氏佐剂组及正常对照组进行比较。结果:与未成模组、弗氏佐剂组及正常对照组相比,成模组小鼠CD4+脾细胞内Treg的水平明显下降(P<0.01),脾细胞Foxp3mRNA的表达降低(P<0.01)。结论:EAMG模型小鼠存在外周免疫耐受缺陷,FoxP3基因可能通过影响Treg的数量和功能在EAMG的发病中起作用。Objective： To study the mechanisms of peripheral immunotolerance disorder in EAMG mice. Methods ： The level of CD4＋ CD25＋ Treg in CD4＋ splenocyte and expression of Foxp3 mRNA in splenocytes of MG symptom group and no MG symptom group were tested and compared with control group. Results： Compared with no MG symptom group, CFA group and control group, the level of CD4＋ CD25＋ Treg of MG symptom group was decreased in splenocytes, expression of Foxp3 mRNA of MG symptom group was decreased in splenocytes. Conclusion： EAMG mice are deficient in peripheral tolerance, which may be in- volved in the development of disease.

关 键 词：EAMG CD4+CD25+调节性T细胞 FOXP3 

分 类 号：R746.1[医药卫生—神经病学与精神病学]