调节性CD4~+T细胞及非调节性CD4~+T细胞与HIV/AIDS患者疾病进展关系的研究

目的分析比较中国HIV感染者CD4+CD25+Foxp3+调节性T细胞(CD4+regulatory T cells,Treg)及非Treg细胞与疾病进展的关系,探讨Treg细胞在HIV感染过程中的作用。方法选取76例HIV/AIDS患者,根据其CD4+T细胞计数水平不同分为3组,A组CD4<200个/μL,B组CD4200～400个/μL,C组CD4>400个/μL。采用流式细胞仪胞内染色技术检测CD4+CD25+Foxp3+调节性T细胞的水平,并分析其与CD4计数及病毒载量的相关性。结果随着疾病的进展,Treg细胞百分比逐渐升高,各组间差异有统计学意义;Treg细胞及非Treg细胞的绝对计数均明显下降,且以非Treg细胞下降为主;Treg绝对计数与病毒载量呈负相关(P<0.05)。结论中国HIV感染者随着疾病进展,辅助性T细胞等非Treg细胞的数量下降,对机体免疫保护能力降低,而Treg细胞数量及功能的下降使其对机体的过度免疫活化的抑制作用减弱,病毒复制,加剧病情进展。

Relationships between Regulatory CD4+ T Cells or Non-regulatory CD4+ T Cells and Disease Progression in HIV/AIDS Patients

Objective To analyze the relationships between CD4⁺CD25⁺Foxp3⁺ regulatory T cells(Treg) or non-CD4⁺CD25⁺Foxp3⁺ regulatory T cells(non-Treg) and disease progression in Chinese HIV-infected individuals,and thereby to investigate the role of Treg in the process of HIV-1-infection.Methods Seventy-six HIV-infected adult patients were enrolled in this study.According to their CD4⁺ T cell counts in peripheral blood,patients were divided into Group A(CD4<200/μL),Group B(CD4 200～400/μL) and Group C(CD4>400/μL),respectively.The CD4⁺CD25⁺Foxp3⁺ regulatory T cells were examined with intracellular staining flow cytometric technique.The relationship between CD4⁺ T cells counts and the plasma HIV-1 viral load was analyzed.Results With the progression of disease the percentages of Treg cells were raised gradually,and this reached statistical significance;compared with the healthy control,both the absolute counts of Treg cells and non-Treg cells decreased significantly in HIV-infected individuals and mainly in the non-Treg cells.Furthermore,the absolute numbers of Treg cells were inversely correlated with plasma HIV-1 RNA viral load(r=-0.334,P<0.05).Conclusion With disease progression in Chinese HIV-1-infected patients,the reduction in the frequency of non-Treg cells,such as helper T cells(Th),dampened the immune protection,while the diminished frequency and function of Treg cells decreased the inhibition of the excessive immune activation,which may favor viral replication and drive HIV disease progression.