肿瘤坏死因子超家族在炎症性肠病中的作用  

Effect of tumor necrosis factor superfamily on inflammatory bowel disease

作　　者：杨贝贝 王丹丹[1] 耿丽 王许平 杜晓博 高闯 冯百岁[1] Yang Beibei;Wang Dandan;Geng Li;Wang Xuping;Du Xiaobo;Gao Chuang;Feng Baisui(Department of Gastroenterology,The Second Affiliated Hospital,Zhengzhou University,Zhengzhou 450014,China)

机构地区：[1]郑州大学第二附属医院消化内科,450014

出　　处：《中华炎性肠病杂志（中英文）》2020年第1期55-58,共4页Chinese Journal of Inflammatory Bowel Diseases

基　　金：国家自然科学基金资助项目(81070288、81270452);河南省自然科学基金项目(162300410268);河南省医学科技攻关计划项目(201502015)。

摘　　要：炎症性肠病(IBD)发病机制尚不明确。肿瘤坏死因子超家族(TNFSF)成员可直接破坏肠道上皮屏障的完整性,共刺激淋巴细胞,从而促进炎症发生发展。肿瘤坏死因子(TNF)可作为IBD治疗的靶标。本文对TNF和其他TNFSF成员,特别是FasL、TRAIL、RANKL、TWEAK、LIGHT和TL1A在IBD发病中的作用进行综述。The pathogenesis of inflammatory bowel disease(IBD)is members of the tumor necrosis factor superfamily(TNFSF)have a role in directly destroying the integrity of the intestinal epithelial barrier and in co stimulating lymphocytes to promote the occurrence and development of inflammation.Tumor necrosis factor(TNF)has a definite pathological role in IBD,and TNF also serves as a target for IBD therapy.This review presents the role of TNF and other TNFSF members,particularly FasL,TRAIL,RANKL,TWEAK,LIGHT and TL1A in the pathogenesis of IBD.

关 键 词：炎症性肠病 肿瘤坏死因子超家族 炎症因子 

分 类 号：R57[医药卫生—消化系统]