摘要
目的 观察严重急性呼吸综合征 (SARS)患者外周血淋巴细胞绝对细胞数和细胞因子在发病过程中的动态变化 ,了解SARS患者机体的免疫状态。方法 用酶联免疫吸附法 (ELISA)动态检测 2 1例SARS患者发病过程中血浆细胞因子IFN α、TNF α、IFN γ、IL 12和IL 10的水平。结果 分别有 6 6 7%的患者外周血淋巴细胞绝对细胞数、38 1%的患者血浆IFN α水平和 6 1 9%的患者血浆TNF α水平在发病中期达到高峰。部分患者Th1细胞因子IL 12和IFN γ有所升高 ,而所有患者整个检测时间内Th2细胞因子IL 10的产生未受到影响。 85 7%的患者发病后血浆IFN α的首次检测值 (16 1 0 9± 132 6 9pg/ml)显著低于正常值 (86 7 18± 30 6 5 0 pg/ml,P <0 0 5 )。结论 SARS病毒感染后机体的免疫反应在病程中期可能最强 ,且可能以Th1反应为主。血浆IFN α首次检测值显著低于正常值的特征可作为SARS早期诊断的依据。
Objective To investigate the immunological status of patients with SARS by monitoring the dynamic changes in peripheral blood lymphocyte count and plasma levels of cytokines. Methods Levels of IFN α,TNF α, IFN γ, IL 12 and IL 10 in plasma of 21 SARS patients were sequentially assayed with enzyme linked immunosorbent assay (ELISA) Lymphocyte count of peripheral blood was also determined. Results Peripheral blood lymphocyte counts in 66 7% of patients, plasma IFN α level in 38 1% of patients, and plasma TNF α level in 61 9% of patients showed inverted V shaped profiles, with peaks in the middle of SARS course. Production of Th2 cytokine IL 10 was not influenced in the present study in all patients, while high levels of Th1 cytokines IL 12 and IFN γ were observed during the observation period in some patients. The first detected values of IFN α. In 85 7% of patients, the levels of IFN α at the onset of symptoms were much lower than those in normal controls (867 18±306 50pg/ml; P <0 01), and the mean concentration of it of all SARS patients (161 09±132 69) was also lower than that in normal controls ( P <0 01). Conclusion These results suggest that the immune response may be active in the middle of SARS course and a Th1 response may be dominant during SARS virus infection. The characteristic low IFN α level at the onset of the disease might be used as an early diagnostic indicator for SARS virus infection
出处
《解放军医学杂志》
CAS
CSCD
北大核心
2003年第11期994-997,共4页
Medical Journal of Chinese People's Liberation Army
基金
全军医学科研"十五"计划指令性课题 (编号 0 3F0 1 7)
北京市自然科学基金 (编号 70 340 51 )资助课题