EB病毒潜伏期膜蛋白1诱发系统性红斑狼疮可能机制的探讨  

The study on the possible pathogenesis of EBV latent membrane protein 1 in inducing systemic lupus erythematosus

作　　者：王丽芹[1] 王吉波[1] 潘琳[1] 梁宏达[1] 辛苗苗[1] 董静[1] 

机构地区：[1]青岛大学医学院附属医院风湿免疫科,266003

出　　处：《中华风湿病学杂志》2011年第10期707-709,共3页Chinese Journal of Rheumatology

基　　金：山东省自然科学基金（Y2007C037）;山东省医药卫生科研项目（HW027）

摘　　要：目的探讨EB病毒潜伏期膜蛋白1（LMPI）诱发系统性红斑狼疮（SLE）的可能机制。方法应用实时荧光定量聚合酶链反应（PCR）检测SLE患者及健康对照外周血单个核细胞（PBMCs）的LMP1、凋亡相关基因bcl-2、baxmRNA表达水平，酶联免疫吸附试验（ELISA） 法检测B细胞活化因子（BAFF）水平。采用，检验进行阳性率比较，采用2-△Ct法比较各基因表达水平，采用Student—Newman—Kqeuls法进行均数间两两比较。结果①SLE患者组LMP1阳性率为25％，显著高于健康对照组的11％（P=O．03）。②SLE组bcl-2mRNA表达水平2-△Ct值为0．0257，对照组为0．0183，差异有统计学意义。③SLE组LMP1阳性患者bcl-2mRNA表达水平2-△Ct值为0．0427，而LMP1阴性患者为0．0217，差异有统计学意义。④SLE组LMPI阳性患者、LMP1阴性患者，健康对照组LMP1阳性者,LMP1阴性者血清BAFF水平分别为（106±15）、（82±19）、（68±19）、（64-±17）μg／L，SLE组LMP1阳性患者与其余3组比较差异均有统计学意义（P均〈0．01），SLE组LMP1阴性患者与健康对照2组比较差异有统计学意义（P〈0．01）。结论EB病毒可能通过LMP1影响凋亡相关基因bcl-2表达、诱导B细胞产生BAFF，导致被感染的自身反应性B细胞存活延长而促发SLE发生发展。Objective To investigate the possible pathogenesis of EB virus （EBV） latent membrane protein 1 in inducing systemic＇lupus erythematosus （SLE）. Methods The mRNA expression levels of LMP1 and apoptosis-related： genes bcl-2, bax in SLE patients and healthy controls were detected by real-time fluorescence quantitative polymerase chain reaction （PCR）. The serum BAFF levels of SLE patients and normal healthy controls were detected by ELISA. 2 test was used for positive rate analysis, 2-△Ct method was used for comparing the gene expression level, and Student-Newman-Kqeuls method was used for pair-wise comparison between the means. Results （1） The positive rate of LMP1 expression in 67 SLE cases was 25%, which was significantly higher than the 11% in 65 healthy controls （P〈0.05）. （2） The 2-△Ct value of bcl-2 mRNA expression level of SLE patients was 0.0257, 1.41 times to that （0.0183） of healthy controls and the difference was statistically significant. （3） The 2-△Ct value of bcl-2 mRNA expression level of LMP1 positive SLE patients was 0.0427, 1.98 times to that of LMP1 negative SLE patients （0.0217）, the difference was statistically significant. （4） The serum BAFF levels of LMP1 positive SLE patients, LMP1 negative SLE patients, LMP1 positive healthy controls and LMPI negative healthy controls were （106±15）, （82±19）, （68± 19）, （64±17） μg/L, respectively. There were significant differences between serum BAFF levels of LMP1- positive SLE patients and other groups（P〈0.01 ）. There were significant difference between serum BAFF levels of LMP1-negative SLE patients and the control groups （P〈0.01）. Conclusion EBV may induce and/or promote SLE by LMP1 through apoptosis-related genes bcl-2 expression and induction of B lymphocytes that produce BAFF, all these mechanisms can prolong the infected auto-reactive B lymphocytes survival.

关 键 词：红斑狼疮 系统性 疱疹病毒4型 人 基因 BCL-2 B淋巴细胞活化因子 

分 类 号：R593[医药卫生—内科学]