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作 者:韩云坤[1] 孙冰[2] 李丽红[1] 孙利炜[1]
机构地区:[1]长春市儿童医院,吉林长春130051 [2]解放军装甲兵技术学院门诊部,吉林长春130117
出 处:《中国实验诊断学》2011年第9期1533-1536,共4页Chinese Journal of Laboratory Diagnosis
摘 要:目的探讨川崎病(Kawasaki disease,KD)时细胞免疫功能及一些细胞因子在疾病发生发展中的变化。方法 2003年1月-2007年10月在我院住院的KD患者52例、热性对照42例、正常对照30例,采用酶联免疫吸附试验(enzyme-linked immunosorbent assay,ELISA)检测三组血清巨噬细胞迁移抑制因子(macrophage migration inhibitory factor,MIF)、白细胞介素-6(interleukin-6,IL-6)、肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)、白细胞介素-1β(interleukin-1β,IL-1β),采用流式细胞术检测川崎病患者的细胞免疫功能。其中川崎病患者分别于急性期(发病第1-11天)与亚急性期(发病第11-21天)各检测一次。结果川崎病急性期T淋巴细胞CD4无明显变化,CD8比例减少,CD4/CD8比值明显增高(P<0.01);川崎病患儿急性期血清MIFI、L-6、TNF-αI、L-1β水平明显升高(P<0.01);川崎病患儿亚急性期血清MIFI、L-6、TNF-αI、L-1β水平较急性期明显下降(P<0.01);川崎病同一个体不同病程期间,血清MIF和IL-6水平有很好的相关性,特别是急性期患儿二者呈正相关(r=0.87,P=0.017)。结论川崎病急性期细胞免疫系统处于活化状态,活化的T细胞分泌高浓度的炎性细胞因子如IL-1I、L-6、MIF和TNF-α等,引起一系列的血管炎性改变和脏器损伤。检测血清MIF和IL-6水平,可望作为川崎病患儿急性期的一个判断指标。Objective This study expored the changes of T cell function and some cytokines in KD.Methods Serum samples were collected from 52 patients with KD,30 normal healthy subjects,and 42 febrile control subjects,respectively.The serum levels of CD3,CD4 and CD8 positive T cell was detected by flow cytometry.Cytokines,including MIF,IL-6,TNF-α and IL-1β were assayed by ELISA.Results The absolute counts of CD3+ and CD4+ T cells had no obvious changes while the absolute counts of CD8+ T cells decreased in KD during the acute stage,and the level of CD4/CD8 increased observably.There was a significant increase in the serum levels of MIF,TNF-α,IL-6 and IL-1β in the acute stage of KD compared with those in the subacute stage(P〈0.01) and normal controls(P〈0.001),and febrile controls(p = 0.01).And there was also a correlation between the serum levels of MIF and IL-6 in patents with KD,especially in the acute stage(r=0.87,P=0.017).Conclusion There was a activation of peripheral blood T cells immune function,especially the increasing level of CD4/CD8 at the acute stage in KD,this lead to the secretion of a lot of cytokines,such as MIF,IL-6,TNF-α and IL-1β,these cytokines were involved in the pathology and pathogenesis cause of KD.
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