CD4+CD25+FoxP3+调节性T细胞与结核病的关系

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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,提示天然诃节性T细胞可能参与结核病的发生。 Objective To investigate the status of CD4 ~ + CD25 ~ + FoxP3 ~ + regulatory T cells in patients with tuberculosis and the relationship between the expression of FoxP3 and its pathogenesis. METHODS: Forty-five patients with active tuberculosis (including 25 pulmonary tuberculosis and 20 tuberculous lymphadenitis), 20 healthy controls, 20 recovered tuberculosis and 6 patients with cervical lymph node hyperplasia were enrolled. Flow cytometry was used to detect the expression of CD4 ~ + CD25 ~ + FoxP3 ~ + regulatory T cells and FoxP3 in peripheral blood. FoxP3 mRNA expression was detected by quantitative RT-PCR and FoxP3 protein expression in lymphoid tissues was detected by immunohistochemistry. Results The proportion of natural regulatory T cells in peripheral blood of patients with active tuberculosis was 2.91% ± 0.23%, significantly higher than that of healthy controls (1.22% ± 0.18%) and recovered TB patients (1.50% ± 0.17%, P <0.01) . The proportion of FoxP3 positive cells in CD4 ~ + CD25 ~ + cells was higher than that in healthy controls. The levels of FoxP3 mRNA in peripheral blood mononuclear cells of tuberculosis patients were significantly higher than those in healthy controls (P <0.05). Immunohistochemistry showed that the expression of FoxP3 in tuberculous lymphadenitis was significantly higher than that in reactive hyperplasia (P <0.01). Conclusions T regulatory cells are significantly increased in patients with tuberculosis, suggesting that natural hematopoietic T cells may be involved in the pathogenesis of tuberculosis.
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