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作 者:苟紫菱 王永俊[2] 卢放根[2] 张洁[2] Gou Ziling;Wang Yongjun;Lu Fanggen;Zhang Jie(Department of Gastroenterology,the Fourth Affiliated Hospital of Southwest Medical University(People's Hospital of Meishan Tianfu New Area),Meishan 620564,China;Department of Gastroenterology,the Second Xiangya Hospital,Digestive Disease Research Institute,Central South University,Changsha 410011,China)
机构地区:[1]西南医科大学附属第四医院(眉山天府新区人民医院)消化内科,眉山620564 [2]中南大学湘雅二医院消化内科,中南大学消化病研究所,长沙410011
出 处:《中华炎性肠病杂志(中英文)》2024年第6期473-479,共7页Chinese Journal of Inflammatory Bowel Diseases
摘 要:克罗恩病(CD)是一种可累及全消化道的慢性透壁性肠道炎性疾病。病因不明,主要认为是环境、遗传易感性和肠道菌群等多种因素导致的胃肠黏膜免疫炎症反应。研究发现白细胞介素23/辅助性T细胞17(IL-23/Th17)炎症轴在CD中桥接固有免疫和适应性免疫,通过IL-23 p19-JAK-STAT3通路使初始T细胞向Th17分化,产生以IL-17为代表的大量促炎细胞因子,从而维持肠道炎症。该轴受遗传基因、肠道菌群和胆汁酸代谢调控。现已开发出针对IL-23/Th17炎症轴的部分信号分子的药物,取得良好的疗效。未来可深入开发该轴的潜在靶点药物,这将有益于CD的个性化治疗。Crohn's disease(CD)is a chronic transmural inflammatory bowel disease that can affect the entire digestive tract.The etiology is unknown,but it is mainly considered to be caused by a variety of factors such as environment,genetic susceptibility,and gut microbiota,leading to immune-inflammatory reactions in the gastrointestinal mucosa.Studies have found that the interleukin 23(IL-23)/T helper cell 17(Th17)inflammatory axis in CD bridges innate immunity and adaptive immunity,promoting the differentiation of naive T cells into Th17 through the IL-23p19-JAK-STAT3 pathway,producing a large amount of pro-inflammatory cytokines represented by IL-17,thereby maintaining intestinal inflammation.This axis is regulated by genetic genes,gut microbiota,and bile acid metabolism.Drugs targeting some signaling molecules of the IL-23/Th17 inflammatory axis have been developed and have achieved good therapeutic effects.In the future,further development of potential target drugs for this axis will be beneficial to personalized treatment of CD.
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