再生障碍性贫血患者B细胞及其介导的体液免疫状况研究

B Lymphocytes and Humoral Immunity in Patients with Aplastic Anemia

目的观察再生障碍性贫血(AA)患者B细胞及其介导的体液免疫状况。方法 AA患者65例,其中非重型再生障碍性贫血(NSAA)35例,重型再生障碍性贫血(SAA)30例,同期正常体检者25名(正常组)。速率散射比浊法检测AA组与正常组免疫球蛋白(Ig G、Ig A及Ig M)含量,比较免疫球蛋白表达情况。流式法检测AA组与正常组CD20+、CD19+CD38+、CD5+CD19+比例。结果(1)AA组和正常组患者各免疫球蛋白浓度差异无统计学意义(P>0.05);SAA患者Ig A、Ig M、Ig G浓度低于NSAA患者(1.46g/L比1.97g/L,P<0.05;1.47g/L比1.50g/L,P<0.05;10.80g/L比11.05g/L,P<0.05);(2)AA组B淋巴细胞亚群中CD20+比例明显低于正常组(9.00%比12.12%,P<0.05);CD19+CD38+、CD19+CD5+比例明显高于正常组(6.23%比3.80%,P<0.05;2.43%比1.90%,P<0.05);SAA和NSAA患者CD20+比例差异无统计学意义(P>0.05),SAA患者CD19+CD38+、CD19+CD5+比例明显高于NSAA患者(6.80%比4.40%,P<0.05;7.35%比1.80%,P<0.05);(3)AA患者强化免疫抑制治疗(IST)无效患者CD19+CD38+、CD19+CD5+比例均高于治疗有效患者(12.30%比4.53%,P<0.05;7.70%比1.93%,P<0.05)。结论 AA患者存在B淋巴细胞介导的体液免疫紊乱,B淋巴细胞功能紊乱的AA患者对IST疗效差。

Objective To investigate the changes and clinical significance of B-lymphocyte subsets and the humoral immunity in aplastic anemia（AA） patients. Methods Sixty-five AA patients were recuited in this study, of which 35 were non-severe AA（NSAA） patients and 30 were severe AA（SAA） patients. Twenty-five healthy subjects served as controls. Rate immune scatter turbidimetry was used to detect the concentration of immunoglobulin（Ig A,Ig M and Ig G） in AA patients and controls. Flow cytometry assay was used to determine the expression of CD20＋B lymphocytes, activated CD19＋CD38＋B lymphocytes, and B lymphocyte subset CD5＋CD19＋. Results No significant difference in immunoglobulin concentrations was found between AA group and control group（P0.05）, while the concentrations of Ig A, Ig M, and Ig G in SAA group were lower than those in NSAA group（1.46 g/L vs 1.97 g/L; 1.47 g/L vs 1.50 g/L; 10.80 g/L vs 11.05 g/L; all P0.05）. The expression of CD20＋B lymphocytes in AA group was significantly lower than that of control group（9.00% vs 12.12%, P0.05）; the expression of CD19＋CD38＋, CD19＋CD5＋B lymphocytes in AA group was significantly higher than that of control group（6. 23 % vs 3. 80 %; 2. 43 % vs1.90%; all P 0.05）; no difference in CD20 ＋B lymphocytes expression was noted between SAA group and NSAA group（P0.05）, but CD19＋CD38＋, CD19＋CD5＋B lymphocytes expression in SAA group were higher than those in NSAA group（6.80% vs 4.40%; 7.35% vs 1.80%; P0.05）. AA patients who were responding to immunosuppressive therapy had a significantly lower expression of CD19＋CD38＋, and CD19＋CD5＋B lymphocytes than those of transfusion dependent patients（4.53% vs 12.30%; 1.93% vs 7.70%; all P0.05）. Conclusion B lymphocytes mediated humoral immune disorder exists in AA patients, and the patients with dysfunction B lymphocytes show poor therapeutic effect.