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目的 探讨严重急性呼吸综合征 (SARS)患者病情进展的宿主免疫机制。方法 使用流式细胞仪检测急性SARS感染患者 5 0例和正常对照 2 0例的细胞因子 (IL 2、IL 4、IL 6、IL 10、IFN γ、TNF α)。按照疾病预后分成死亡组和治愈组 ,前瞻性设计分析细胞因子在 2组患者中的异同及对病情发展的影响。结果 治愈组与死亡组患者的细胞因子 (IL 2、IL 4、IL 6、IL 10、IFN γ、TNF α)均明显高于正常对照组 ,差异有显著性 (P <0 .0 5 )。治愈组和死亡组比较 :治愈组IFN γ高于死亡组 ,差异有显著性 (P <0 .0 5 ) ,死亡组IL 6、IL 10明显高于治愈组 ,差异有显著性 (P <0 .0 5 )。结论 SARS病毒感染确实引起机体的免疫系统紊乱。功能受损的程度与疾病的预后有一定相关性 ;TH2类细胞因子免疫反应过强 ,TH1类细胞因子免疫反应相对减弱 ,造成的机体免疫自稳平衡失调可能是SARS患者死亡的因素之一
Objective To investigate the host immune mechanism in patients with severe acute respiratory syndrome (SARS). Methods Flow cytometry was used to detect cytokines (IL 2, IL 4, IL 6, IL 10, IFN γ, TNF α) in 50 SARS patients and 20 normal controls. According to the prognosis of the disease were divided into death group and the cure group, prospective design analysis of cytokines in two groups of similarities and differences and the impact on the progression of the disease. Results The levels of cytokines (IL 2, IL 4, IL 6, IL 10, IFN γ, TNF α) in the cured and dead patients were significantly higher than those in the normal control group (P <0.05). Compared with the death group, the levels of IFN-γ in the cured group were significantly higher than those in the death group (P <0.05), and the levels of IL-6 and IL-10 in the death group were significantly higher than those in the cured group .0 5). Conclusion SARS virus infection does cause the body’s immune system disorder. The extent of impaired function is related to the prognosis of the disease. The immune response of TH2-type cytokines is too strong, the immune response of TH1-type cytokines is relatively weakened, and the imbalance of immune homeostasis may be one of the factors of SARS death