Abstract: Objective To explore the expression and its significance of CD4+CD25+ regulatory T cells (Tr) in pathogenesis of chronic abacterial prostatitis patients (CAP). Methods 20 CAP patients and 10 volunteers were taken into this study and their peripheral blood was collected for testing the Tr through flow cytometry. Foxp3, the important regulatory factor of Tr, was detected by RT-PCR. The Tr’ cytokines including IL-10 and TGF-β1 in both peripheral blood (PB) and prostatic fluid(PF) were measured by ELISA. Routine blood tests (BT), C-reaction protein (CRP) and erythrocyte sedimentation rate (ESR) were also compared as the inflammatory indexes. Results Compared with the volunteers, percentage of Tr in the CAP patients was significantly lower so was the Foxp3 (P=0.013 and 0.000 respectively). About the cytokines, the IL-10 and TGF-β1 in both PB and PF of the CAP group were significantly lower than that in the volunteers, so was the monocyte in PB (MONO). But there was no statistically difference of WBC, NEU, LYM, CRP and ESR between the two groups. Pearson correlation analysis showed that MONO correlated with the quantities of Tr, Foxp3, IL-10 and TGF-β1. Conclusion Decreased Tr resulting insufficient of immunodepression and degressive IL-10 causing proliferation of MONO, which leaded to the excessive antigen presenting and immune injury, maybe a key role in pathogenesis of chronic abacterial prostatitis.

摘要： 摘要 目的 观察调节性T细胞(Treg)在慢性无菌性前列腺炎(CAP)发病机制的作用及意义。方法 使用流式细胞术检测20例CAP患者及10例健康志愿者外周血Treg的数量；用RT-PCR法检测Treg 的调节蛋白Foxp3mRNA的表达含量；用ELISA法两组前列腺按摩液细胞因子白介素-10（IL-10）及转化生长因子-β1(TGF-β1)的含量；同时比较两组血常规、C-反应蛋白(CRP)及血沉(ESR)的比较。结果 与健康志愿者比较，CAP患者外周血Treg数量及Foxp3mRNA表达含量明显降低(P=0.013,0.000)；细胞因子方面，CAP患者外周血及前列腺液IL-10及TGF-β1均显著低于志愿者；两组的白细胞(WBC)、中性粒细胞(NEU)、淋巴细胞(LYM)、CRP及ESR均无组间差异；但CAP组患者单核细胞(MONO)明显高于志愿者；相关性分析表明患者单核细胞与Treg、Foxp3、IL-10及TGF-β1呈显著正相关性。结论 Treg数量降低所致的免疫抑制不足，其细胞因子IL-10减少所致MONO数量增加、抗原提呈过度导致免疫反应过强，可能是CAP的重要免疫学机制。

关键词: 调节性T细胞, 细胞因子, 慢性前列腺炎, 免疫机制, 单核细胞, Regulatory T cells, Cytokines, Chronic abacterial prostatitis, Immune mechanism, Monocyte