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初发SLE病人Th1/Th2及调控因子IL-18基因研究 被引量:4

Studying on Th1/Th2 and their regulatory cytokines in SLE patients
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摘要 目的:探讨未经药物治疗初发狼疮病人Th1/Th2细胞亚群分布及其调控细胞因子、细胞因子受体基因表达的差异,试图揭示系统性红斑狼疮发病的免疫紊乱机理。方法:运用三色荧光标记法流式细胞术检测42例未经药物治疗初发狼疮病人细胞亚群分布,并以10例正常人作对照;ABI7700 real-time PCR法同时检测 38例未经药物治疗初发狼疮病人和 28例正常人IL-18及其受体mRNA表达水平的差异。结果:①初发狼疮病人Th1较正常人明显减低(P<0.05),但Th1/Th2无显著性改变。②与正常组相比,SLE组病人IL-18 mRNA及其受体表达较正常人明显降低(P<0.05);③面部红斑组病人Th1/Th2较正常人明显降低(P<0.05);④关节炎组SLE病人较无关节炎病人IL-18表达降低。结论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。 Abstract Objective:To analyze Th1/Th2 balance of peripheral Th cells and its inducing cytokines and cytokine receptors in recent onsetSLE patients to make clear the cause of the immunological imbalance in SLE patients. Methods: The intracellular cytokine detection methodwith flow cytometry was used to quantitates Th1/Th2 cells in recent-onset SLE patient(n=42) and the control(n=10) .At the same time,using ABI 7700 real time PCR to detect IL-18, IL-18R mRNA expression in SLE patoemts(n=38/42) and the control(n=28). Results:There were no difference in the Th1/Th2 ratio between SLE patients and the control (P>0.05). However,Th1 was decreased significantly inthe SLE patient group than that in the normal control (P<0.05) .IL-18 and their according receptor IL-18R significantly decreased in SLEgroup than that in the control(Pall < 0.05). SLE patients with malar rash group has the significantly lower Th1/Th2 ratio. Conclusion: SLE isa relative Th2 predominance disease due to the Th1 decreased and the IL-18 and IL-18R mRNA expression decreased too. SLE patient with ma-lar Th1/Th2 ratio rash maybe the special subtype of the SLE,for they have the different Th distribution and IL-18,IL-18R expression.
出处 《中国免疫学杂志》 CAS CSCD 北大核心 2002年第5期360-364,共5页 Chinese Journal of Immunology
基金 国家自然科学基金(30000154) 上海市科委科技发展基金(01JC14029) 上海市卫生局百人计划项目(99BR007)资助
关键词 系统性红斑狼疮 TH细胞亚群 流式细胞术 细胞因子 real-timePCR法 IL-18基因 Keywords:Lupus erythematosus Recent-onset Th cell Cytokine and receptor Flow cytometry Real-time PCR
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参考文献15

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共引文献17

同被引文献33

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