The study on the possible pathogenesis of EBV latent membrane protein 1 in inducing systemic lupus erythematosus
10.3760/cma.j.issn.1007-7480.2011.10.012
- VernacularTitle: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
- Author:
Liqin WANG
;
Jibo WANG
;
Lin PAN
;
Hongda LIANG
;
Miaomiao XIN
;
Jing DONG
- Publication Type:Journal Article
- Keywords:
Lupus erythematosus,systemic;
Herpesvirus 4,human;
Genes,bcl-2;
BAFF
- From:
Chinese Journal of Rheumatology
2011;15(10):707-709
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the possible pathogenesis of EB virus (EBV) latent membrane protein 1 in inducing systemic lupus erythematosus (SLE).MethodsThe 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.Results① 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).ConclusionEBV 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.
