摘要目的 探讨EB病毒潜伏期膜蛋白1(LMP1)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、bax mRNA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x2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=0.03).②SLE组bcl-2 mRNA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-2 mRNA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LMP1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.

abstractsObjective 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 LMP 1 negative healthy controls were ( 106± 15 ),(82± 19),( 68±19),(64±17) μg/L,respectively.There were significant differences between serum BAFF levels of LMPl-positive SLE patients and other groups(P＜0.0l ).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.