摘要
目的研究肺结核患者外周血中CD4+CD25+FoxP3+调节T细胞是否增多,这些调节T细胞是否抑制结核的特异细胞免疫反应。方法使用细胞分离、流式细胞分析及细胞增殖及增殖抑制等实验方法,对20例肺结核患者及17例健康人群外周血中CD4+CD25+FoxP3+调节T细胞的数量及免疫学特征作研究。结果肺结核患者外周血中CD4+CD25+FoxP3+调节T细胞数占CD4+细胞总数的比例显著高于健康人群(P<0.01)。在体外,肺结核患者外周血单个核细胞在BCG及ESAT-6的刺激下增殖能力比健康对照人群明显增强(P<0.01),产生的γ-干扰素比健康人群也明显增强(P<0.05);清除调节T细胞后的肺结核患者外周血单个核细胞对BCG刺激下产生γ-干扰素及白介素-10比没有清除时显著增强(P<0.05);从肺结核患者外周血分离CD4+CD25+调节T细胞和CD4+CD25-细胞,CD4+CD25-细胞对BCG及ESAT-6刺激产生γ-干扰素和白介素-10的能力因CD4+CD25+调节T细胞加入后而显著减弱(P<0.05)。结论肺结核患者CD4+CD25+FoxP3+调节T细胞增多,通过抑制结核患者细胞免疫反应,参与肺结核的发病。
Objective To determine whether CD4＋CD25＋FoxP3＋regulatory T cells（Treg） are increased in patients with active pulmonary tuberculosis（TB） and whether they suppress specific cellular immune responses.Methods The frequency and the immune function of circulating regulatory T cells were compared in 20 untreated patients with active pulmonary TB and 17 healthy matched control by using cell separation,flow cytometry analysis,proliferation assays and cytokines determination.Results The proportion of CD4＋CD25＋FoxP3＋regulatory T cells within CD4＋ T cells was significantly increased in the blood of active pulmonary TB patients than heathy control subjects（P0.01）.Responsing to both Bacille Calmette Guerin（BCG） and early secretory antigenic target-6（ESAT-6）,the peripheral blood mononuclear cells（PBMCs） of pulmonary TB patient had significantly higher cellular proliferation compared to the PBMCs from healthy donors（both P0.01）,and had higher IFN-γ production（both P0.05）.PBMCs from pulmonary TB patient had significantly higher BCG-induced IFN-γ and IL-10 production after CD4＋CD25＋regulatory T cells depletion than before（both P0.05）.CD4＋CD25-cells isolated from TB patients had significantly lower BCG-stimulated and ESAT-6-stimulated IFN-γ production and IL-10 production with CD4＋CD25＋ T cells from TB patients than in the cells without CD4＋CD25＋ T cells（both P0.05）.Conclusion CD4＋CD25＋FoxP3＋ regulatory T cells are expanded in patients with active pulmonary TB,and therefore contribute to the pathogensis of human TB by suppressing specific Mycobacterium tuberculosis cellular immune responses.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2011年第20期2124-2127,共4页
Journal of Third Military Medical University
基金
重庆市自然科学基金(CSTC2007BB5293)~~
