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2
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World J Gastroenterol. 2016 Nov 28;22(44):9706-9717. doi: 10.3748/wjg.v22.i44.9706.
3
IL-33 treatment attenuated diet-induced hepatic steatosis but aggravated hepatic fibrosis.白细胞介素-33治疗减轻了饮食诱导的肝脂肪变性,但加重了肝纤维化。
Oncotarget. 2016 Jun 7;7(23):33649-61. doi: 10.18632/oncotarget.9259.
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Interleukin-33 drives hepatic fibrosis through activation of hepatic stellate cells.白细胞介素-33 通过激活肝星状细胞驱动肝纤维化。
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本文引用的文献

1
Interleukin-33 drives hepatic fibrosis through activation of hepatic stellate cells.白细胞介素-33 通过激活肝星状细胞驱动肝纤维化。
Cell Mol Immunol. 2018 Apr;15(4):388-398. doi: 10.1038/cmi.2016.63. Epub 2017 Feb 13.
2
Interleukin-33 in the pathogenesis of liver fibrosis: alarming ILC2 and hepatic stellate cells.白细胞介素-33在肝纤维化发病机制中的作用:警示2型固有淋巴细胞和肝星状细胞
Cell Mol Immunol. 2017 Feb;14(2):143-145. doi: 10.1038/cmi.2016.62. Epub 2016 Dec 26.
3
Galectin-3 and IL-33/ST2 axis roles and interplay in diet-induced steatohepatitis.半乳糖凝集素-3与白细胞介素-33/ST2轴在饮食诱导的脂肪性肝炎中的作用及相互作用
World J Gastroenterol. 2016 Nov 28;22(44):9706-9717. doi: 10.3748/wjg.v22.i44.9706.
4
Hypoxia inducible factor-1α-induced interleukin-33 expression in intestinal epithelia contributes to mucosal homeostasis in inflammatory bowel disease.缺氧诱导因子-1α诱导肠道上皮细胞中白细胞介素-33的表达有助于炎症性肠病中的黏膜稳态。
Clin Exp Immunol. 2017 Mar;187(3):428-440. doi: 10.1111/cei.12896. Epub 2016 Dec 6.
5
IL-33 Contributes to Schistosoma japonicum-induced Hepatic Pathology through Induction of M2 Macrophages.IL-33 通过诱导 M2 巨噬细胞促进日本血吸虫病引起的肝病理变化。
Sci Rep. 2016 Jul 21;6:29844. doi: 10.1038/srep29844.
6
Role of IL-33 expression in oncogenesis and development of human hepatocellular carcinoma.白细胞介素-33表达在人类肝细胞癌发生发展中的作用。
Oncol Lett. 2016 Jul;12(1):429-436. doi: 10.3892/ol.2016.4622. Epub 2016 May 25.
7
Ablation of interaction between IL-33 and ST2+ regulatory T cells increases immune cell-mediated hepatitis and activated NK cell liver infiltration.白细胞介素-33与ST2+调节性T细胞之间相互作用的消融会增加免疫细胞介导的肝炎以及活化的自然杀伤细胞在肝脏中的浸润。
Am J Physiol Gastrointest Liver Physiol. 2016 Aug 1;311(2):G313-23. doi: 10.1152/ajpgi.00097.2016. Epub 2016 Jun 23.
8
Insulin resistance in development and progression of nonalcoholic fatty liver disease.胰岛素抵抗在非酒精性脂肪性肝病发生发展中的作用
World J Gastrointest Pathophysiol. 2016 May 15;7(2):211-7. doi: 10.4291/wjgp.v7.i2.211.
9
Relevance of serum interleukin-33 and ST2 levels and the natural course of chronic hepatitis B virus infection.血清白细胞介素-33和ST2水平与慢性乙型肝炎病毒感染自然病程的相关性
BMC Infect Dis. 2016 May 16;16:200. doi: 10.1186/s12879-016-1543-x.
10
IL-33 treatment attenuated diet-induced hepatic steatosis but aggravated hepatic fibrosis.白细胞介素-33治疗减轻了饮食诱导的肝脂肪变性,但加重了肝纤维化。
Oncotarget. 2016 Jun 7;7(23):33649-61. doi: 10.18632/oncotarget.9259.

IL-33-ST2 轴在肝脏疾病中的作用:进展与挑战。

IL-33-ST2 Axis in Liver Disease: Progression and Challenge.

机构信息

Center of Non-Infectious Liver Diseases, Peking University 302 Clinical Medical School, Beijing, China.

Center of Non-Infectious Liver Diseases, Beijing 302 Hospital, Beijing, China.

出版信息

Mediators Inflamm. 2017;2017:5314213. doi: 10.1155/2017/5314213. Epub 2017 Oct 18.

DOI:10.1155/2017/5314213
PMID:29180837
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5664344/
Abstract

The new member of the IL-1 family, interleukin-33 (IL-33), participates in the progression of a variety of diseases through binding with its receptor ST2. Recently, much clinical evidence and experimental data have indicated that IL-33 is associated with various liver diseases. This review primarily addresses the relationship between IL-33 and several hepatic diseases. IL-33 can alleviate high-fat diet- (HFD-) induced hepatic steatosis and insulin resistance, and IL-33 acts as an alarmin, which quickly triggers the immune system to respond to virus invasion and toxic damage to the liver. However, when liver injury is chronic, IL-33 promotes Th2 reactions and hepatic stellate cell (HSC) activity, facilitating progression to liver fibrosis. The complicated functions of IL-33 should be considered before its clinical application.

摘要

白细胞介素-33(IL-33)是白介素-1 家族的新成员,通过与其受体 ST2 结合参与多种疾病的进展。最近,大量的临床证据和实验数据表明,IL-33与各种肝脏疾病有关。本综述主要探讨了 IL-33 与几种肝疾病的关系。IL-33 可减轻高脂饮食(HFD)诱导的肝脂肪变性和胰岛素抵抗,并且 IL-33 作为警报素,可迅速触发免疫系统对病毒入侵和肝毒性损伤做出反应。然而,当肝损伤为慢性时,IL-33 促进 Th2 反应和肝星状细胞(HSC)活性,促进肝纤维化进展。在 IL-33 的临床应用之前,应该考虑其复杂的功能。