首页> 中文期刊> 《检验医学》 >强直性脊柱炎患者外周血中B淋巴细胞亚群、B细胞活化因子及其受体的表达研究

强直性脊柱炎患者外周血中B淋巴细胞亚群、B细胞活化因子及其受体的表达研究

         

摘要

目的 研究强直性脊柱炎(AS)患者外周血中B淋巴细胞亚群、B细胞活化因子(BAFF)及其受体BP3的表达,为进一步探讨AS发病机制提供新的理论依据.方法 采用流式细胞术测定24例AS患者及30名正常健康体检者外周血中CD19+总B细胞、CD19+ CD20+ CD27 -初始B细胞、CD19+ CD20+ CD27+记忆性B细胞、CD19+ CD38+抗体分泌细胞、BAFF及其受体BR3的表达百分率;采用免疫散射比浊法测定AS患者和正常体检者血清免疫球蛋白IgG、IgA、IgM浓度;并分析外周血白细胞BAFF的表达水平与B淋巴细胞亚群百分率、免疫球蛋白浓度之间的相关性.结果 与正常对照组比较,AS患者的外周血中CD19+总B细胞和CD19+CD38+抗体分泌细胞的表达率、BAFF及其受体BR3的表达比例、血清IgG、IgA浓度均明显升高(P<0.05).外周血白细胞中BAFF的表达水平分别与外周血白细胞CD19+总B细胞、CD19+ CD38+抗体分泌细胞百分率及血清IgG、IgA浓度呈明显正相关(r=0.695,P=0.000;r =0.610,P=0.002;r =0.813,P=0.000;r=0.665,P=0.000).结论 AS患者外周血中存在异常表达的总B细胞、抗体分泌细胞、BAFF及其受体BR3,提示在AS的发病过程中,B淋巴细胞的异常表达及活化可能发挥致病作用.%Objective To investigate the expressions of B lymphocyte subsets, B-cell activating factor (BAFF) and its receptor BR3 in peripheral blood from patients with ankylosing spondylitis ( AS) , and provide the reference for the further research of AS pathological mechanism. Methods A total of 24 AS patients and 30 healthy subjects were enrolled in the research. The expression percentages of CD19+ total B cells, CD19+ CD20+ CD27- native B cells, CD19+ CD20+ CD27+ memory B cells, CD19+ CD38+ plasmablast B cells, BAFF and its receptor BR3 were determined by flow cytometry. The concentrations of serum immunological proteins ( IgG, IgA and IgM) were determined by nephelometry. The correlation of BAFF expression, B lymphocyte subset percentages and immunological protein concentration was analyzed. Results The results showed that the expressions of CD19+ total B cells, CD19+ CD38+ plasmablast B cells, BAFF and receptor BR3 and the concentrations of serum IgG and IgA in AS patients were significantly higher than those of healthy controls (P < 0. 05 ). The expression of BAFF was correlated with the percentages of CD19+ total B cells, CD19+ CD38+ plasmablast B cells, serum concentrations of IgG and IgA (r = 0.695,P= 0.000; r = 0.610, P=0.002; r=0.813, P=0.000; r=0.665, P=0.000). Conclusions The aberrant expressions of total B cells, plasmablast B cell, BAFF and receptor BR3 may be involved in the pathogenesis of AS.

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