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目的:观察实验性抗磷脂综合征(experimental anti-phospholipid antibody syndrome,EAPS)进展过程中小鼠CD4+CD25+调节性T细胞(CD4+CD25+Treg)数量和功能变化。方法:以重组人β2糖蛋白1(rhβ2GP1)主动免疫BALB/c小鼠建立实验性APS模型,免疫12周后检测抗β2糖蛋白1抗体(anti-β2-GP1)、抗心磷脂抗体(ACA)、流产率(%)、活化部分凝血活酶时间(aPTT)、血小板计数(PLT PBC)。以流式细胞术检测小鼠PBMC中CD4+CD25+Treg细胞频率,RT-PCR检测转录因子Foxp3 mRNA的表达水平。结果:模型小鼠anti-β2-GP1、aCL水平明显升高,aPTT延长,PLT PBC降低,流产率提高,差异有统计学意义(P<0.05)。模型小鼠PBMC中foxp3基因表达在4周短暂高于对照组(P<0.05),8周后随着APS进展开始逐渐降低,12周后明显低于对照组(P<0.05)。PBMC中CD4+CD25+Treg细胞频率8周前与对照组相比差异无统计学意义(P>0.05),12周后逐渐减少,明显低于对照组(P<0.05)。结论:CD4+CD25+Treg数量和功能下降参与抗磷脂综合征的发病机制。
Objective: To observe the changes of CD4 + CD25 + regulatory T cells (CD4 + CD25 + Treg) in mice with experimental anti-phospholipid antibody syndrome (EAPS). Methods: BALB / c mice were immunized with recombinant human β2 glycoprotein 1 (rhβ2GP1) to establish an experimental APS model. Anti-β2-GP1 and anti-cardiolipin antibodies (ACA ), Abortion rate (%), activated partial thromboplastin time (aPTT), and platelet count (PLT PBC). The frequency of CD4 + CD25 + Treg cells in PBMC of mice was detected by flow cytometry, and the expression of Foxp3 mRNA was detected by RT-PCR. Results: The levels of anti-β2-GP1 and aCL in model mice were significantly increased, prolongation of aPTT, decrease of PLT PBC and increase of miscarriage rate were found in the model mice (P <0.05). The expression of foxp3 gene in PBMC of model mice was transiently higher than that of the control group at 4 weeks (P <0.05). After 8 weeks, the expression of foxp3 gene gradually decreased with the progression of APS and was significantly lower than that of the control group after 12 weeks (P <0.05). The frequency of CD4 + CD25 + Treg cells in PBMC was not significantly different from that in the control group 8 weeks before (P> 0.05), but gradually decreased after 12 weeks, which was significantly lower than that in the control group (P <0.05). Conclusion: The number and function of CD4 + CD25 + Treg are involved in the pathogenesis of antiphospholipid syndrome.