il-9及tl1a在溃疡性结肠炎患者肠黏膜组织中的表达变化

il-9及tl1a在溃疡性结肠炎患者肠黏膜组织中的表达变化

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时间:2018-10-16

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1、授予单位代码10089学号或申请号20153157中国图书分类号R574.62HebeiMedicalUniversity硕士学位论文专业学位IL-9及TL1A在溃疡性结肠炎患者肠黏膜组织中的表达变化研究生段洋洋导师张晓岚教授霍晓霞副主任医师专业内科学二级学院第二医院2018年3月目录中文摘要············································································································1英文摘要·····

2、·······································································································3英文缩写············································································································5研究论文IL-9及TL1A在溃疡性结肠炎患者肠黏膜组织中的表达变化前言·············

3、······························································································6材料与方法·······························································································7结果···································································

4、······································20附图·········································································································25附表·········································································································37讨论·····

5、····································································································38结论·········································································································39参考文献··················································

6、···············································40综述肿瘤坏死因子超家族成员在Th9细胞分化中的作用························42致谢··················································································································51个人简历···········································

7、·······························································52中文摘要IL-9及TL1A在溃疡性结肠炎患者肠黏膜组织中的表达变化摘要溃疡性结肠炎(ulcerativecolitis,UC)发病机制不明,多数学者认为免疫因素是其主要发病机制。Th9细胞是一种新发现的CD4+T细胞亚群,主要分泌白细胞介素9(Interleukin-9,IL-9),PU.1是其特异性转录因子。研究证实,Th9细胞及IL-9参与UC发生发展,并成为研究热点。肿瘤坏死因子样配体1A(

8、tumornecrosisfactorligand-relatedmolecule1A,TL1A)是TNFSF15编码的蛋白产物,GWAS研究证实TNFSF15是UC的易感基因。研究发现UC患者中TL1A表达明显升高,并与肠道炎症程度呈正相关。TL1A过表达慢性实验性结肠炎模型中,TL1A

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