【摘要】 目的探讨哮喘患者外周血血清程序性细胞死亡因子-1(PD-1)、γ干扰素(IFN-γ)、白细胞介素-4(IL-4)及辅助性T细胞(Th细胞)的表达。方法以江苏省连云港市第一人民医院呼吸内科收治的41例哮喘患者为研究对象,依据病情分为急性发作组(20例)和慢性持续组(21例),另选18例健康者作为对照组。患者在起病入院时抽取外周血,采用酶联免疫吸附法检测PD-1、IFN-γ、IL-4的浓度,流式细胞仪检测外周血Th1、Th2及Th1/Th2的表达。结果与健康对照组比较,慢性持续组、急性发作组外周血PD-1、IFN-γ浓度降低,IL-4浓度升高,Th1细胞比率、Th1/Th2比值降低,Th2细胞比率升高,差异均有统计学意义(均P<0.05)。与慢性持续组比较,急性发作组外周血PD-1、IFN-γ浓度更低,IL-4浓度更高,Th1细胞比率、Th1/Th2比值更低,Th2细胞比率更高,差异均有统计学意义(均P<0.05);急性发作组PD-1与IFN-γ、Th1呈正相关(r值分别为0.678和0.712,均P<0.05),与IL-4、Th2呈负相关(r值分别为–0.745和–0.700,均P<0.05)。结论哮喘患者外周血PD-1降低,急性发作组更低,且与常规的哮喘检测指标呈相关性。更多还原

【Abstract】 Objective To investigate the expression of programmed cell death-1(PD-1), interferon-γ(IFN-γ),interleukin-4(IL-4) and T help cells(Th) in peripheral blood of patients with asthma. Methods Forty-one asthma patients were divided into an acute group(20 cases) and a chronic group(21 cases) according to the disease state of asthma. Another 18 healthy subjects were recruited as a control group. Peripheral blood samples were collected from all the subjects at admission or inclusion. The concentrations of PD-1, IFN-γ and IL-4 were detected by enzyme-linked immunoassay method. The expressions of Th1 and Th2 were detected by flow cytometry method. Results The PD-1 and IFN-γ concentrations, Th1 proportion and Th1/Th2 ratio in the two asthma groups were reduced compared with the healthy control group, and were significantly lower in the acute group compared with the chronic group(all P<0.05). The IL-4 level and Th2 proportion in the two asthma groups were increased compared with the healthy control group, and were significantly higher in the acute group than the chronic group(all P<0.05). In the acute group, the PD-1 level was positively correlated with IFN-γ and Th1 level(r values were 0.678 and 0.712, respectively), and negatively correlated with IL-4 and Th2(r values were –0.745 and –0.700, respectively). Conclusion The concentration of PD-1 in patients with asthma is reduced especially in acute asthma, and shows close correlation with conventional index of asthma.更多还原