初发SLE患者Th1/Th2及IL-10、IL-18基因的表达

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探讨初发狼疮病人Th1/Th2分布及其调控细胞因子、细胞因子受体基因表达的差异。运用三色荧光标记法流式细胞术检测 35例未经药物治疗初发狼疮病人T细胞亚群分布 ,并以 10例正常人作对照 ;同时运用ABI770 0TagManRealTime定量PCR法检测其中 38例病人和 2 8例正常人IL 10、IL 18及其受体、IL 10 /IL 18mRNA表达的差异。结果 :(1)初发狼疮病人Th1较正常人明显减低 (P <0 0 5 ) ,但Th1/Th2无显著性改变 ;(2 )与正常组相比 ,SLE组病人IL 10mRNA表达无显著性差异 ,但IL 10R表达明显升高 (P <0 0 5 ) ;SLE组病人IL 18mRNA及其受体表达较正常人明显降低 (P值均 <0 0 5 ) ;(3)面部红斑组病人Th1/Th2较正常组降低 (P均 <0 0 5 ) ,IL 10R较正常组显著增高 (P <0 0 5 ) ;(4)RNP阳性组病人IL 10、较正常组升高 (P均 <0 0 5 ) ,IL 18降低 ;(5 )关节炎组病人IL 18R较无关节炎病人显著降低。SLE是一种以Th1细胞下降 ,Th2细胞相对占优势的免疫介导的自身免疫性疾病 ,源于诱导向Th1细胞分化的IL 18及其受体减少和细胞因子间失衡所致。 To investigate the distribution of Th1 / Th2 in patients with first-onset lupus and the differences in the expression of cytokines and cytokine receptors. The distribution of T lymphocyte subsets in 35 patients without initial treatment of lupus was detected by three-color fluorescence-labeled flow cytometry and 10 normal controls were used as control. At the same time, 38 patients and 38 normal controls were detected by ABI770 0 TagMan Real Time quantitative PCR Difference of IL 10, IL 18 and its receptor, IL 10 / IL 18 mRNA expression in 8 normal subjects. Results: (1) Compared with normal controls, the Th1 / Th2 levels in patients with first onset lupus were significantly lower than those in normal controls (P <0.05); (2) Compared with normal controls, the levels of IL 10 mRNA in patients with SLE were not significantly different (P <0.05). The expression of IL-18 mRNA and its receptor in SLE patients was significantly lower than that in normal subjects (all P <0.05). (3) Th1 (P <0 05), IL 10R was significantly higher than that of the normal group (P <0.05); (4) The level of IL 10 in RNP positive group was significantly higher than that in the normal group 0 5), IL 18 decreased; (5) patients with arthritis group IL 18R was significantly lower than non-arthritis patients. SLE is an immune-mediated autoimmune disease that is characterized by a decrease in Th1 cells and a relative predominance of Th2 cells, resulting from the induction of IL 18 and its receptors that differentiate into Th1 cells and the imbalance between cytokines.
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