调节性B细胞在免疫性血小板减少症患者中的表达及意义

W. Qian, Xiaoxia Zhang
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摘要

目的:探讨调节性B细胞在免疫性血小板减少症患者中的表达及意义。方法:73例ITP患者分为糖皮质激素治疗组(42例)和重组人血小板生成素(rhTPO)治疗组(31例)。根据疗效分为有效组和无效组。采用流式细胞术检测治疗前后外周血CD19+ CD24hiCD38hi Breg的表达。采用ELISA法检测治疗前后转化生长因子(TGF)-β1、白细胞介素(IL-10)、干扰素(IFN)-γ的表达水平。选取30名志愿者作为对照组。结果:73例ITP患者治疗前CD19+ CD24hiCD38hi Breg及细胞因子IL-10、TGF-β1表达均低于对照组,IFN-γ表达高于对照组(p < 0.05)。05). 有效组CD19+ CD24hiCD38hi Breg、IL-10、TGF-β1表达水平均显著高于治疗前,IFN-γ表达水平均显著低于治疗前(p < 0.05)。05). 无效组CD19+ CD24hiCD38hi Breg、IFN-γ、IL-10、TGF-β1的表达与治疗前比较无明显变化。结论:CD19+ CD24hiCD38hi Breg及相关细胞因子的异常表达参与了ITP的发病机制。
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Expression and Significance of Regulatory B Cells in Patients with Immune Thrombocytopenia
Objective: To detect the expression and significance of regulatory B cells in patients with immune thrombocytopenia. Methods: 73 ITP patients were divided into glucocorticoids treatment group (n = 42) and recombinant human thrombopoietin (rhTPO) treatment group (n = 31). According to the thera-peutic effect, it was divided into effective group and ineffective group. The expression of CD19+ CD24hiCD38hi Breg in peripheral blood was detected by flow cytometry before and after treatment. The expression levels of transforming growth factor (TGF)-β1, interleukin (IL-10) and interferon (IFN)-γ were detected by ELISA before and after treatment. 30 volunteers were se-lected as the control group. Results: The expression of CD19+ CD24hiCD38hi Breg and cytokines IL-10 and TGF-β1 in 73 ITP patients before treatment was lower than that in the control group, while the expression of IFN-γ was higher than that in the control group (p < 0. 05). The expression levels of CD19+ CD24hiCD38hi Breg, IL-10 and TGF-β1 in the effective group were significantly higher than before treatment, while the expression of IFN-γ was significantly lower than before treatment (p < 0. 05). The expression of CD19+ CD24hiCD38hi Breg, IFN-γ, IL-10 and TGF-β1 in the invalid group had no significant change compared with before treatment. Conclusion: Abnormal expression of CD19+ CD24hiCD38hi Breg and related cytokines is involved in the pathogenesis of ITP.
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