肾虚型类风湿关节炎与B淋巴细胞人免疫球蛋白GFc段受体Ⅱ b的相关性研究

目的探索B淋巴细胞（B细胞）人免疫球蛋白G Fc段受体Ⅱ b（Fcgamma receptor Ⅱ b， FcγRⅡ b）的表达与肾虚型类风湿关节炎（rheumatoid arthritis，RA）的相关性。方法 RA患者43例，其中肾虚型26例，非肾虚型17例，采用流式细胞术检测外周血幼稚B细胞、记忆B细胞和前浆细胞表达FcγR Ⅱ b的水平，分析压痛关节数、肿胀关节数、血沉（ESR）、类风湿因子（RF）和病情活动指数评分（DAS28）与B细胞分布及FcγR Ⅱ b表达水平的相关性；另设健康志愿者对照21名。结果肾虚型RA外周血记忆B细胞及前浆细胞FcγR Ⅱ b表达分别为（49.65%±15.86%）及（43.69%±22.57%），比健康对照组［（64.03%±6.01%）及（66.59%±10.18%）］显著下调（P<0.01）；非肾虚型RA记忆B细胞FcγR Ⅱ b表达［（52.70%±9.52%）］比健康对照组明显下调（P<0.01）；肾虚型RA前浆细胞FcγR Ⅱ b表达明显低于非肾虚组［（56.10%±17.05%）］，差异有统计学意义（P<0.05）；B细胞亚群FcγRⅡ b表达与压痛关节数、肿胀关节数、ESR、RF和DAS28评分无相关性。结论肾虚型RA 患者B细胞免疫失耐受可能与记忆B细胞及前浆细胞表达FcγRⅡ b下调密切相关，肾虚型RA可能存在FcγRⅡ b基因的异常从而导致自身免疫失耐受。

英文摘要:

Objective To study the correlation between the expression of Fcgamma receptorⅡ b （FcγRⅡ b） on B cells and rheumatoid arthritis （RA） patients of Shen deficiency syndrome （SDS）. Methods There were 43 RA patients， including 26 of SDS and 17 of non SDS. The expression levels of FcγRⅡ b on naive B cells， memory B cells， and plasma blasts in the peripheral blood were detected by flow cytometry. The numbers of tender joints， numbers of swollen joints， erythrocyte sedimentation rate （ESR）， rheumatoid factor （RF）， and disease activity score （DAS28）， the correlation between the distribution of B cells and the expression level of FcγRⅡ b in RA patients were analyzed. Besides， another 21 healthy volunteers were recruited as the control group. Results The expression level of FcγRⅡb was 49.65%±15.86% on memory B cells and 43.69%±22.57% on plasma blasts in RA patients of SDS， significantly down regulated when compared with those of the control group （64.03%±6.01%， 66.59%±10.18%， P<0.01）. The expression level of FcγRⅡb on memory B cells of RA patients of non SDS was down regulated more obviously when compared with that of the control group （52.70%±9.52% versus 64.03%±6.01%， P<0.01）. The expression level of FcγRⅡb on plasma blasts was obviously lower in RA patients of SDS than in RA patients of non SDS （56.10%±17.05%，P<0.05）. The expression level of FcγRⅡ b on memory B cells was not correlated with numbers of tender joints， numbers of swollen joints， ESR， RF， or DAS28. ConclusionsThe defective immunological tolerance of B cells in RA patients of SDS might be closely correlated with down regulation of FcγRⅡb on memory B cells and plasma blasts. There might exist genetic abnormality of FcγRⅡ b gene in RA patients of SDS， thus inducing loss of autoimmunity tolerance.

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