非酒精性脂肪性肝炎的免疫发病机制

刘静; 施军平

非酒精性脂肪性肝炎的免疫发病机制

刘静,
施军平

1. 浙江中医药大学
2. 浙江中医药大学附属杭州第六医院

基金项目:

国家自然科学基金(81070316)；浙江省自然科学基金(Y2101436)；

详细信息

中图分类号: R575.1
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- 被引次数: 0
出版历程
- 出版日期: 2012-05-20

The immune pathogenesis of nonalcoholic steatohepatitis

Research funding:

摘要

摘要: <正>在非酒精性脂肪性肝病(NAFLD)漫长的病程中,非酒精性脂肪性肝炎(NASH)是单纯脂肪肝发生肝硬化的限速步骤。"二次打击"学说的发病机制为大多数学者所接受[1],但其并不能解释所有的问题。近年来免疫系统在NASH发病中的作用越来越受到重视,肝脏免疫与NASH的关系成为当前国内外
- 脂防肝
- fatty liver

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参考文献(28)

[1]Baffy G.Kupffer cells in non-alcoholic fatty liver disease:Theemerging view[J].J Hepatol, 2009, 51 (1) :212-223.

[2]Gao B, Radaeva S, Park O.Liver natural killer and natural kil-ler T cells:immunobiology and emerging roles in liver disea-ses[J].J Leukoc Biol, 2009, 86 (3) :513-528.

[3]Miura K, Seki E, Ohnishi H, et al.Role of Toll-Like recep-tors and their downstream molecules in the development ofnonalcoholic fatty liver disease[J].Gastroenterol Res Pract, 2010, 2010:362847.

[4]Zhan YT, An W.Roles of liver innate immune cells in nonal-coholic fatty liver disease[J].World J Gastroenterol, 2010, 16 (37) :4652-4660.

[5]Koek GH, Liedorp PR, Bast A.The role of oxidative stress innon-alcoholic steatohepatitis[J].Clin Chim Acta, 2011, 412:1297-1305.

[6]Otagawa K, inoshita K, Fujii H, et al.Erythrophagocytosis byliver macrophages (Kupffer cells) promote oxidative stress, inflammation, and fibrosis in a rabbit model of steatohepatitis[J].Am J Pathol, 2007, 170 (3) :967-980.

[7]CaniPD, Amar J, Iglesias MA, et al.Metabolic endotoxemiainitiates obesity and Insulin resistance[J].Diabetes, 2007, 56 (7) :1761-1772.

[8]Tilg H.The Role of Cytokines in non-alcoholic fatty liver dis-ease[J].Dig Dis, 2010, 28 (1) :179-185.

[9]Adler M, Taylor S, Ckebugeu K, et al.Intrahepatic natural killerT cell populations are increased in human hepatic steatosis[J].World J Gastroenterol, 2011, 17 (13) :1725-1731.

[10]Maher JJ, Leon P, Ryan JC.Beyond insulin resistance:In-nate immunity in non-alcoholic steatohepatitis[J].Hepatol-ogy, 2008, 48 (2) :670-678.

[11]Kremer M, Thomas E, Milton RJ, et al.Kupffer cell and In-terleukin-12-Dependent loss of nature killer T cell in hepa-tosteatosis[J].Hepatology, 2010, 51 (1) :130-141.

[12]Ma X, Hua J, Li Z.Probiotics improve high fat diet-inducedhepatic steatosis and insulin by increasing hepatic NKT cells[J].Hepatology, 2008, 49 (5) :821-830.

[13]Kahraman A, Schlattjan M, Kocabayoglu P, et al.Major his-to-compatibility complex class I-related chains A and B (MIC A/B) :a novel role in nonalcoholic steatohepatitis[J].Hepatology, 2010, 51 (1) :92-102.

[14]Rada eva S, Sun R, Jaruga B, et al.Natural killer cells amel-iorate liver fibrosis by killing activated stellate cells in NKG2D-dependent and tumor necrosis factor-related apoptosis-inducing ligand-dependent manners[J].Gastroenterology, 2006, 130 (2) :435-452.

[15]Jeong WI, Gao B.Innate immunity and alcoholic liver fibrosis[J].J Gastroenterol Hepatol, 2008, 23 (1) :S112-S118.

[16]Rensen S, Slaats Y, Driesen A, et al.Activation of the com-plement system in human nonalcoholic fatty liver disease[J].Hepatology, 2009, 50 (6) :1809-1817.

[17]Yu H, Yang Y, Zhang M, et al.Thyroid status influence onAdiponectin, acylation stimulation protein (ASP) and comple-ment C3 in hyperthyroid and hypothyroid subject[J].NutrMetab, 2006, 3:13.

[18]Yesilova Z, Ozata M, Oktenli C, et al.Increased acylationstimulating protein concentrations in nonalcoholic fatty liverdisease are associated with insulin resistence[J].Am JGastroenterol, 2005, 100 (4) :842-849.

[19]Hillebrandt S, Wasmuth HE, Weiskirchen R, et al.Comple-ment factor 5 is a quantitative trait gene that modifies liver fi-brogenesis in miceandhumans[J].Nat Genet, 2005, 37 (8) :835-843.

[20]Wang Y, Yang YX.Advances in understanding the role ofcomplement in the pathogenesis of fatty liver disease[J].World J Dig, 2010, 18 (15) :1577-1581.

[21]Winer S, Chan Y, Paltser G, et al.Normalization of obeisity-associated insulin resistance throgh immunotherapy[J].Nat med, 2009, 15 (8) :921-929.

[22]Ma X, Hua J, Mohamood AR, et al.A High-Fat Diet andRegulatory T cell influence susceptibility to endotoxin-in-duced liver injury[J].Hepatology, 2007, 46:1519-1529.

[23]Sakaguchi S, Yamaguchi T, Nomura T, et al.Regulatory T celland immune tolerance[J].Cell, 2008, 5 (9) :775-787.

[24]Federico A, Aiuto ED, Borriello F, et al.Fat:A matter ofdisturbance for the immune system[J].World J Gastroen-terol, 2010, 16 (38) :4762-4772.

[25]Ogura H, Murakani M, Okuyama Y, et al.Interleukin-17promotes autoimmunity by triggering a positive-feedbackloop via interleukin-6 induction[J].Immunity, 2008, 29 (4) :628-636.

[26]Shi PQ, Zhu S, Qian YC.IL-17 signaling and function[J].Chinese Journal of cell Biology, 2011, 33 (4) :345-357.

[27]Tang Y, Bian Z, Zhao L, et al.Interleukin-17 exacerbates he-patic steatosis and inflammation in non-alcoholic fatty liver dis-ease[J].Clin EXP Immunol, 2011, 166 (2) :281-290.

[28]Starley BQ, Calcagno CJ, Harrison SA.Nonalcoholic fatty liv-er disease and hepatocellular carcinoma:a weighty connec-tion[J].Hepatology, 2010, 51 (5) :1820-1832. (本文编辑:王莹

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