中文摘要：

目的探讨结核病患者中CD4^＋CD25^＋FoxP3^＋调节性T细胞存在状态、功能相关蛋白FoxP3表达水平及其与发病的关系。方法纳入对象包括45例活动性结核患者（包括25例肺结核和20例结核性淋巴结炎）、20例健康对照、20例康复的结核及6例颈淋巴结反应性增生患者。流式细胞术检测外周血中CD4^＋CD25^＋FoxP3^＋调节性T细胞及其FoxP3蛋白的表达强度；荧光定量RT-PCR检测FoxP3 mRNA表达；免疫组化检测淋巴组织中FoxP3蛋白表达。结果活动性结核患者外周血中天然调节性T细胞的比例为2．91％±0．23％，显著高于健康对照（1．22％±0．18％）和康复的结核患者（1．50％±0．17％，P〈0．01），FoxP3阳性细胞在CD4^＋CD25^＋细胞中的比例高于健康对照，结核患者外周血单个核细胞中FoxP3 mRNA水平显著高于健康对照（P〈0．05）。免疫组化显示，结核性淋巴结炎组织中FoxP3的表达显著高于反应性增生的淋巴结组织（P〈0．01）。结论结核患者调节性T细胞显著增高，提示天然调节性T细胞可能参与结核病的发生。

英文摘要：

Objective To investigate the frequency of CD4^＋CD25^＋FoxP3^＋ regulatory T cells （Treg） and the expression of the functional protein, FoxP3, in patients with active tuberculosis and the relationship between Treg and the pathogenesis of tuberculosis. Methods Forty five patients with active tuberculosis （including 25 cases of pulmonary tuberculosis and 20 tuberculous lymphadenitis）, 20 healthy controls, 20 recovered tuberculosis patients and 6 patients with reactive hyperplasia in cervical lymph node were enrolled. The frequency of CD4^＋CD25^＋FoxP3^＋ Treg in the peripheral blood was measured by flow cytometry. FoxP3 mRNA expression was determined by real-time reverse transcriptase-polymerase chain reaction （RT-PCR） and the expression of FoxP3 protein in lymphoid tissues was measured by immunohistochemistry. Results The frequency of natural Treg in the peripheral blood from the patients with active tuberculosis was 2.91% ± 0. 23%, which was significantly higher than that of healthy control group （1. 22%± 0. 18%） and recovered tuberculosis patients （1. 50% ±0. 17%, P 〈 0.01）. FoxP3^＋ cells in CD4^＋CD25^＋ T cells and FoxP3 mRNA expression in peripheral blood mononuclear cell（PBMC） of patients with active tuberculosis were both much more than those in healthy controls （P 〈 0.05）. The expression of FoxP3 detected by immuno- histochemistry in lymph nodes of patients with tuberculous lymphadenitis was much higher than that in the reactive hyperplasia lymphoid tissues. Conclusion CD4^＋CD25^＋FoxP3^＋ Treg expansion in patients with active tuberculosis indicates that Treg may be involved in the pathogenesis of tuberculosis.