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目的观察结核性胸膜炎患者调节性T细胞(Treg细胞)、辅助性T细胞17(Th17)以及相关细胞因子水平变化情况,分析其在疾病发病机制中的作用。方法 43例结核性胸膜炎患者为研究组,43例入院进行健康检查者为对照组。取两组研究对象静脉血,分别对Treg、Th17细胞含量进行测定,同时检测相关因子水平,对检查结果进行分析。结果对照组Th17、Th17/Treg值、Treg分别为(0.76±0.13)%、(0.14±0.03)、(5.17±0.74)%,研究组Th17、Th17/Treg值、Treg分别为(1.24±0.23)%、(0.27±0.06)、(4.28±0.62)%;研究组Th17、Th17/Treg值高于对照组,Treg细胞含量低于对照组,差异均有统计学意义(P<0.05)。对照组白细胞介素(IL)-6、转化生长因子-β(TGF-β)、IL-17分别为(3.86±0.52)、(3.75±0.63)、(13.74±2.62)ng/L,研究组IL-6、TGF-β、IL-17分别为(4.96±0.84)、(3.52±0.75)、(18.04±3.62)ng/L;两组TGF-β水平比较差异无统计学意义(P>0.05),研究组IL-6、IL-17因子水平高于对照组,差异有统计学意义(P<0.05)。结论 Th17及Treg细胞通过其本身及分泌相关细胞因子在结核性胸膜炎的发病过程中可能起着重要作用。
Objective To observe the changes of regulatory T cells (Tregs), helper T cells (Th17) and related cytokines in patients with tuberculous pleurisy and to analyze their roles in the pathogenesis of the disease. Methods Forty-three patients with tuberculous pleurisy were studied, and 43 were admitted to hospital for health check-up. Venous blood was taken from two groups of subjects, and the contents of Treg and Th17 cells were respectively measured. Meanwhile, the levels of related factors were measured and the results were analyzed. Results Th17, Th17 / Treg and Treg in control group were (0.76 ± 0.13)% and (5.17 ± 0.74)%, respectively. The values of Th17, Th17 / Treg and Treg in study group were (1.24 ± 0.23) %, (0.27 ± 0.06) and (4.28 ± 0.62)%, respectively. The Th17 and Th17 / Treg values in the study group were higher than those in the control group, and the contents of Treg cells in the study group were lower than those in the control group (P <0.05). The levels of IL-6, TGF-β and IL-17 in the control group were (3.86 ± 0.52), (3.75 ± 0.63) and (13.74 ± 2.62) ng / L, (4.96 ± 0.84), (3.52 ± 0.75) and (18.04 ± 3.62) ng / L, respectively. There was no significant difference in the levels of TGF-β between the two groups (P> 0.05 ). The levels of IL-6 and IL-17 in the study group were significantly higher than those in the control group (P <0.05). Conclusion Th17 and Treg cells may play an important role in the pathogenesis of tuberculous pleurisy through their own and secretion related cytokines.