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作 者:叶霜[1] 沈南[1] 顾越英[1] 陈顺乐[1] 韩光明[1] 冯修高[1] 冯学兵[1] 陈兴国[1] 华晶[1] 黄文群[1] 王元[1] 鲍春德[1]
机构地区:[1]上海第二医科大学附属仁济医院风湿科上海市风湿病研究所,200001
出 处:《中华风湿病学杂志》2002年第6期411-416,I002,共7页Chinese Journal of Rheumatology
基 金:国家自然科学基金资助项目 (3 0 0 0 0 15 4) ;上海市科技发展基金资助项目 (0 1JC14 0 2 9)
摘 要:目的 通过基因表达谱勾画系统性红斑狼疮 (SLE)发病机制中可能的免疫调控通路。方法 用寡核苷酸基因芯片研究了 10例SLE(包括 2例SLE同胞对 )和 10份正常对照的外周血白细胞基因表达谱。进行了基因表达谱和临床免疫表型的聚类分析和比较 ;筛选统计学显著性差异表达的SLE相关基因 ,并在转录和蛋白表达水平验证芯片表达谱结果。结果 聚类分析揭示SLE临床免疫表型与基因表达谱特征存在关联。获得 2 5个显著性差异表达的SLE相关基因 ,其中大部分未经报道。转录水平直接验证了其中C/EBPD ,LY6E ,OAS2三个基因的表达 ;较大样本独立验证了C/EBPD ,LY6E在SLE中的表达上调 ;蛋白质水平验证了C/EBPD的高表达。结论 SLE基因表达谱可能是其临床免疫表型的分子基础 ,探讨了通过基因表达谱进行SLE分型乃至鉴别诊断的可能性。通过显著性差异表达的SLE相关基因 ,推测干扰素及其免疫调控通路在SLE发病中可能扮演重要角色。Objective To delineate the immune regulatory pathway in pathogenesis of systemic lupus erythematosus (SLE) by using gene expression profile analysis.Methods Peripheral white blood cell gene expression profile of 10 SLE patients,including one SLE sib pair,was determined by oligonucleotide microarray.Ten chips from normal population were served as controls.Clustering of gene expression profile and clinical immune phenotype were performed and compared.SLE associated statistically significant genes were determined,and validated at both transcript and protein expression level.Results There was certain relationship between expression profiling and immune phenotype clusters.Twenty five disease associated genes were found,some of which are novel in that they have not been related to SLE before.Among these genes,C/EBPD,Ly6E and OAS2 were directly confirmed by real time PCR.In addition,C/EBPD and Ly6E were validated in a much larger population.Furthermore,upregulated protein expression of C/EBPD in SLE was obtained.Conclusion Gene expression profile seems to be the molecular basis of diverse immune phenotypes of SLE.There are possibilities to determine subtypes of this disease by expression profile analysis,even help to make differential diagnosis in the long run.From SLE associated genes it has been suggested that there are clues highly indicating that IFN and its regulatory pathway may play an important role in the etiology of SLE.
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