抗CD20抗体治疗慢性特发性血小板减少性紫癜机制的研究

目的:通过抗CD20抗体(Rituximab,商品名:美罗华)与慢性特发性血小板减少性紫癜(cITP)骨髓体外培养,了解cITP患者B细胞的活化与凋亡的状况。方法:选择cITP患者30 例,对照组缺铁性贫血患者10例,进行骨髓体外培养,于培养前、培养3 d、培养6 d、培养9 d,检测B细胞相关分子(CD19、CD20、CD23)和透射电镜观测淋巴细胞凋亡状态。结果:cITP患者骨髓CD20、CD23分子表达显著高于对照组CD20、CD23分子表达(P<0.01)。加抗CD20抗体和加半量抗CD20抗体培养前后B细胞相关分子(CD19、CD20、CD23)检测结果差异有统计学意义(P<0.01)。加抗CD20抗体组透射电镜观测有淋巴细胞凋亡。结论:抗CD20 抗体能靶向性地与表达CD20抗原的B细胞结合,通过抗体抗原反应,诱导B细胞加速凋亡。

Study on the mechanism of Rituximab in treating patients with chronic idiopathic thrombocytopenic purpura

Objective:To investigate B cells activation and apoptosis by culturing marrows of patients with chronic idiopathic thrombocytopenic purpura in vitro with anti-CD20 monoclonal antibody (Rituximab).Method:We chose 30 chronic idiopathic thrombocytopenic purpura patients and 10 iron deficiency anemia patients as control to do in vitro marrow culture. We detected B cell-associated molecules (CD19, CD20, CD23) and observed lymphocyte apoptosis by using transmission electron microscope before culture and 3, 6, 9 days after culture.Result:The expression of molecule CD20, CD23 in marrows of patients with chronic idiopathic thrombocytopenic purpura was significantly higher than that of patients with iron deficiency anemia (P< 0.01). The B cell-associated molecule (CD19, CD20, CD23) in group of adding full-dose anti-CD20 monoclonal antibody and half-dose anti-CD20 monoclonal antibody had significant difference before and after culture (P< 0.01). We found lymphocyte apoptosis in group of adding full-dose anti-CD20 monoclonal antibody by using transmission electron microscope.Conclusion:Rituximab can bind to B cells which express CD20 antigen and induce B cell apoptosis by antigen-antibody reaction.