FcγRIIB下调在肾虚型类风湿关节炎B细胞活化中的作用

Role of FcγRIIB down regulation in B cell activation of RA with kidney deficiency

目的:通过对肾虚型类风湿关节炎患者B细胞活化情况与FcγRIIB表达分析,揭示FcγRIIB在肾虚型类风湿关节炎B细胞活化中的作用机制。方法:纳入RA患者共57例,记录一般情况、临床资料(疾病活动情况,自身抗体水平),收集外周血单核细胞(PBMC),Ig M刺激培养48 h后流式细胞法检测CD86与FcγRIIB表达情况。结果:肾虚型RA患者幼稚B细胞的CD86表达率明显较非肾虚型患者高,同时FcγRIIB的MFI较非肾虚型患者低;肾虚型RA患者记忆B细胞的FcγRIIB表达率明显较幼稚B细胞低,且肾虚型RA患者ACPA水平越高其记忆B细胞的FcγRIIB表达率越低。结论:肾虚型RA患者存在FcγRIIB水平的下调,其能够促进B细胞过度活化和自身抗体水平升高。

Objective:To investigate the B cells activation and the expression of FcγRIIB in patients with kidneydeficiency type of rheumatoid arthritis(RA),it would reveal the mechanism of FcγRIIB in kidney-deficiency type of rheumatoid arthritis.Methods:There were 57 RA patients totally.They were classified into kidney deficiency type and nokidney deficiency type according to the diagnostic criteria of TCM syndromes.Collecting the general condition,disease activity,auto-antibody level,in addition,2 ml blood samples were collected from the patients and extracted the peripheral blood monocytes(PBMC)from the blood samples.After 48 hours of Ig M stimulation,fluorescence staining was performed,then the expression of CD86 and FcγRIIB was detected by flow cytometry.Result:The expression rate of CD86 in the kidney deficiency group on naive B cells was significantly higher than that of no-kidney deficiency group,and the MFI of FcγRIIB was lower than that of the no-kidney deficiency groups.In kidney deficiency group,the expression rate of FcγRIIB in memory B cells was significantly lower than that in naive B cells.Moreover,the higher ACPA level of patients with kidney deficiency,the lower FcγRIIB expression rate of memory B cells.Conclusion:The reduction of FcγRIIB in the kidney deficiency of RA patients,which may lead to over-activation of B cells and increased levels of auto-antibodies.