B细胞刺激因子在系统性红斑狼疮患者外周血单个核细胞上的表达及意义

目的 探讨B细胞刺激因子(Blys)在系统性红斑狼疮(SLE)患者外周血单个核细胞上的表达情况及临床意义.方法 应用流式细胞仪技术,检测50例SLE患者(其中活动期和稳定期各25例)外周血单个核细胞上Blys的表达,与25例健康献血人员作比较.并分析SLE患者外周血单个核细胞上Blys的表达与病情活动、其他实验指标及自身抗体的关系.结果 SLE患者外周血单个核细胞上表达Blys的百分率上调(P＜0.001),活动期和稳定期SLE患者Blys的表达率均高于健康对照组(P＜0.001和P＜0.05);其中,活动期和稳定期SLE患者比较,活动期患者Blys的表达更高(P＜0.05).SLE患者外周血单个核细胞上Blys的表达水平与SLEDAI评分呈正相关(r=0.702,P＜0.001),与免疫球蛋白IgG、IgM呈正相关(r=0.695,P＜0.001和r=0.356,P＜0.01),与补体C3、C4呈负相关(r=-0.42,P＜0.001和r=-0.31,P＜0.05).dsDNA抗体( )组患者外周血单个核细胞上Blys的表达较dsDNA抗体(-)组高(P＜0.05).Clq抗体( )组患者外周血单个核细胞上Blys的表达也较C1q抗体(-)组高(P＜0.05).结论 Blys在SLE外周血单个核细胞上的表达率升高.Blys的表达在一定程度上反映了病情的活动,并与自身抗体的产生相关.

Expression of Blys on PBMCs from patients with SLE

Objective To investigate the expression of B lymphocyte stimulator (Blys) on peripheral blood mononuclear cells (PBMCs) from patients with systemic lupus erythematosus (SLE), and to analyze their clinical significance.Methods The expression of Blys was measured by flow cytometry on PBMCs from 25 healthy controls and from patients with SLE, who were separated into active group (n=25) and inactive group (n=25) according to the SLE disease activity index (SLEDAI). The relationships between the expression of Blys and several laboratory parameters as well as disease activity were analyzed. Results The expression of Blys on PBMCs from patients with SLE were significantly elevated compared to healthy controls (P<0.001), so did the active group (P<0.001) and inactive group (P<0.05). The expression of Blys on PBMCs from active SLE patients was significantly higher than that of inactive patients (P<0.05). The expression of Blys on PBMCs were positively correlated with SLEDAI, IgG and IgM, but negatively correlated with C3 and C4. The expression of Blys in dsDNA positive group was significantly higher than that of dsDNA negative group (P<0.05). The expression of Blys in C1qAb positive group was significantly higher than that of C1qAb negative group (P<0.05).Conclusion The expression of Blys on PBMCs from SLE is up-regualated. They may involve in the pathogenesis of SLE.