外源性TGF-β1对实验性自身免疫性脑脊髓炎模型小鼠的影响  

Effect of the exogenous transforming growth factor β1 in mouse model of the experimental autoimmune encephalomyelitis

作　　者：吴敏[1] 王玉忠[1] 周文斌[1] 肖波[1] 

机构地区：[1]中南大学湘雅医院神经内科,长沙410008

出　　处：《现代免疫学》2010年第1期68-72,共5页Current Immunology

摘　　要：利用外源性转化生长因子β1（transforming growth factor beta 1,TGF-β1）对实验性自身免疫性脑脊髓炎（experimental autoimmune encephalomyelitis,EAE）发病进行干预,通过检测EAE小鼠T-bet和GATA-3的表达,探讨其可能的作用机制。将72只近交系清洁级8~10周健康雌性C57BL/6小鼠随机分为佐剂组、EAE组、干预组和假干预组,以MOG35-55免疫C57BL/6小鼠制成慢性EAE动物模型,干预组在免疫的同时注射TGF-β1。分别在发病初、高峰期和慢性期,用RT-PCR技术检测各组小鼠T-bet、GATA-3的表达。结果TGF-β1干预组小鼠的发病时间提前、高峰期病情更重,更早进入慢性期,而在慢性期小鼠病情更趋于缓解。干预组小鼠T-bet的表达较佐剂组为高,但较假干预组和EAE组的T-bet表达要低;整个病程中干预组GATA-3的表达均明显低于佐剂组,且较假干预组和EAE组的GATA-3的表达降低更为明显。提示T-bet、GATA-3的变化可反映EAE的免疫失衡状态;外源性TGF-β1在EAE发病中并不是一个单纯的保护性因子,它使高峰期的症状加重,而在慢性期更趋向于缓解。To investigate the effect of the exogenous transforming growth factor β（TGF-β1） on the pathogenesis of the experimental autoimmune encephalomyelitis（EAE） in mouse model and to explore its possible mechanism through the detection of T-bet and GATA-3 expression,72 female C57BL/6 mice of SPF inbred strain,aged 8～10 weeks,were randomly divided into adjuvant group,EAE group,intervention group and group without intervention,while the chronic mouse model of EAE was established by immunization of the C57BL/6 mice with MOG35-55,and TGF-β1 was injected together with the immunization in the intervention group.The expressions of T-bet and GATA-3 in each group of mice were detected in the onset,peak and chronic stage of disease by means of RT-PCR.It was found that the time of onset of disease in the intervention group was shortened,became worse at the peak of disease and went into chronic stage earlier,but the condition in the chronic stage tended to be relieved.The expression of T-bet was higher in the adjuvant group,but lower than those in EAE group and group without intervention.During the whole course of illness the expression of GATA-3 in the intervention group were lower than those of other 3 groups,especially the group without intervention an EAE group of mice.From these observations,it is evident that the expressions of T-bet and GATA reflect the immune imbalance status in EAE,and the exogenous TGF-β1 is not simply a protective factor,but they can make symptom worse at peak of illness and ameliorate the condition in the chronic stage of disease.

关 键 词：实验性自身免疫性脑脊髓炎 转化生长因子Β1 T-BET GATA-3 

分 类 号：R745.44[医药卫生—神经病学与精神病学]