[系统性红斑狼疮患者FcγRIIB1介导的信号异常及B细胞的高活性]

[The abnormality of FcgammaRIIB1-mediated signaling and the hyperactivity of B cells from patients with systemic lupus erythematosus].

作者信息

Peng Ke-Jun, Xiao Lin-Sheng, Fei Ying, Wang Shu-Ren

机构信息

Department of Laboratory Medicine, Chengdu Medical College, Chengdu 610083, China.

出版信息

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2006 Nov;22(6):769-71.

PMID:17077019

Abstract

AIM

To evaluate the effect of FcgammaRIIB(1) (CD32) representative self-inhibitory adjustive mechanism of B cells on pathogenesis of systemic lupus erythematosus (SLE) by observing the expression characteristic and functional state of molecules on the surface of B cells from SLE patients.

METHODS

The peripheral blood mononuclear cells (PBMC) were prepared by density gradient centrifugation, and the B cells were isolated from PBMC by magnetic activated cell sorting (MACS). The fluxes of intracytoplasmic calcium (Ca(2+)) of B cells activated by different activators were measured by fluorescence spectrophotometric method. The IgG production by B cells cultured with activators was assayed by ELISA. The expression levels of CD32, CD19, and IgM on the surface of B cells were measured by flow cytometry.

RESULTS

(1)After B cells were stimulated with goat anti-human mu chain F(ab')(2) fragments and whole IgG respectively, the ratio of Ca(2+) response by F(ab')(2) fragments to whole IgG was significantly lower in SLE B cells compared to rheumatoid arthritis (RA)(P<0.05) or normal (P<0.01) B cells. (2)The ratio of total IgG production by B cells cultured with staphylococcal protein A (SPA) to SPA plus IgG anti-mu chain was significantly lower in SLE patients compared to RA patients or normal individuals (P<0.05). (3)There was no obvious difference in the expression of CD19, CD32, and IgM on the surface of B cells from SLE, RA patients and normal individuals (P>0.05).

CONCLUSION

The inhibitory signaling abnormality of CD32 possibly contributes to the mechanism of hyperactivity of human SLE B cells.

摘要

目的

通过观察系统性红斑狼疮（SLE）患者B细胞表面分子的表达特征和功能状态，评估B细胞代表性的自身抑制调节机制FcγRIIB(1)（CD32）在SLE发病机制中的作用。

方法

采用密度梯度离心法制备外周血单个核细胞（PBMC），通过磁珠激活细胞分选（MACS）从PBMC中分离出B细胞。采用荧光分光光度法检测不同激活剂激活的B细胞胞浆内钙离子（Ca(2+)）通量。采用酶联免疫吸附测定（ELISA）法检测激活剂培养的B细胞产生的IgG。采用流式细胞术检测B细胞表面CD32、CD19和IgM的表达水平。

结果

（1）分别用山羊抗人μ链F(ab')(2)片段和全IgG刺激B细胞后，与类风湿关节炎（RA）（P<0.05）或正常（P<0.01）B细胞相比，SLE B细胞中F(ab')(2)片段与全IgG的Ca(2+)反应比值显著降低。（2）与RA患者或正常个体相比，SLE患者中用葡萄球菌蛋白A（SPA）培养的B细胞产生的总IgG与SPA加抗μ链IgG的比值显著降低（P<0.05）。（3）SLE、RA患者和正常个体B细胞表面CD19、CD32和IgM的表达无明显差异（P>0.05）。