SLE中GATA3和MBD2对IL-4表达的影响  

The influence of GATA3 and MBD2 on the expression of IL-4 in SLE

作　　者：施伟民[1] 秦海红[2] 施若非[1] 伍洲炜[2] 徐金华[3] 郑捷[1] 

机构地区：[1]上海交通大学医学院附属瑞金医院,上海200020 [2]同济大学附属同济医院皮肤科,上海200065 [3]复旦大学附属华山医院皮肤科,上海200040

出　　处：《同济大学学报（医学版）》2007年第3期25-28,共4页Journal of Tongji University(Medical Science)

基　　金：上海市科委课题资助项目(064119529)

摘　　要：目的本文通过检测LE中MBD2、GATA3和IL-4表达的量化关系,探索LE中GATA3和MBD2表达水平对Th2异常分化的影响,旨在探讨基因表达调控异常对LE自身免疫异常的可能机制。方法获取12例系统性红斑狼疮患者和11例健康志愿者外周静脉血单核细胞,以RT-PCR半定量法检测GATA3、MBD2和IL-4的转录水平。采用两样本均数T检验比较分析SLE患者与正常人之间GATA3、MBD2和IL-4转录水平的差异。结果正常对照组PBMC中GATA3表达水平为(0.342±0.117),SLE患者组PBMC中GATA3表达水平为(0.552±0.234),SLE中GATA3表达水平显著高于正常对照(t=1.761,P=0.009);正常对照组MBD2表达水平为(0.587±0.193);SLE患者组MBD2表达水平为(0.760±0.203),SLE中MBD2表达水平显著高于正常对照(t=1.721,P=0.024);正常对照组IL-4表达水平为0.299±0.198;SLE患者组IL-4表达水平为(0.442±0.183),SLE中IL-4表达水平显著高于正常对照(t=1.725,P=0.042)。结论LE中与自身免疫反应有关的Th2细胞活化不仅受到低甲基化造成的IL-4表达增加的影响,而且受到低甲基化造成的沉默因子结合下降的影响,使GATA3失去了MBD2的竞争性抑制,更加有利于诱导IL-4表达,活化Th2,促进LE发病。Objective By quantitative evaluation of the transcription levels of MBD2, GATA3 and IL-4 in lupus erythematosus （LE）, this paper is to explore the possible influence of GATA3 and MBD2 on abnormal differentiation of Th2 and to discuss the possible mechanism of abnormal regulation of gene transcription in autoimmtmity of LE. Methods PBMCs were harvested from 12 SLE patients and 11 healthy controls. The transcription levels of GATA3 ,MBD2 and IL-4 were respectively detected by semiquantitative reverse transcriptase- polymerase chain reaction （RT-PCR）. Student T test was applied for statistical analysis in comparison of transcription levels of GATA3, MBD2 and IL-4 between SLE patients and normal controls. Results The tran-scription level of GATA3 in PBMCs of normal controls was （0. 342 ±0. 117） and that of SLE patients was （0. 552 ± 0. 234）. The transcription level of GATA3 in SLE was significantly higher than that in normal controls （t = 1. 761, P = 0. 009）. The transcription level of MBD2 in PBMCs of normal controls was （0. 587 ± 0. 193） and that of SLE patients was （0. 760 ± 0. 203）, The transcription level of MBD2 in SLE was significantly higher than that in normal controls （t = 1,721, P = 0. 024）. The transcription level of IL-4 in PBMCs of normal controls was （0. 299 ± 0. 198） and that of SLE patients was （0. 442 ± 0. 183）, The transcription level of IL-4 in SLE was significantly more than that in normal controls （ t = 1. 725, P = 0. 042）. Conclusion Activation of Th2 cells in autoimmunity reaction of LE is not only influenced by demethylation that cauls over expression of IL-4, but also affected by decreased combination of regression factors due to demethylation that further make GATA3 avoiding competitive inhibition of MBD2 and accelerating induction of IL-4 expression, activate differentiation of Th2 and promote the pathogenesis of LE.

关 键 词：系统性红斑狼疮 激活因子 沉默因子 

分 类 号：R571[医药卫生—消化系统]