The immunopathogenesis of alcoholic and nonalcoholic steatohepatitis: two triggers for one disease?

被引：60

作者：

Valenti, Luca ^{[1
]}

Fracanzani, Anna Ludovica ^{[1
]}

Fargion, Silvia ^{[1
]}

机构：

[1] Univ Milan, Osped Policlin, IRCCS, Dept Internal Med, I-20122 Milan, Italy

来源：

SEMINARS IN IMMUNOPATHOLOGY | 2009年 / 31卷 / 03期

关键词：

Cytokine; Insulin resistance; Inflammation; Kupffer cell; Steatosis; FATTY-LIVER-DISEASE; TUMOR-NECROSIS-FACTOR; HEPATIC INSULIN-RESISTANCE; TOLL-LIKE RECEPTOR-4; TNF-ALPHA PRODUCTION; SHORT-TERM SURVIVAL; KILLER T-CELLS; ADIPOSE-TISSUE; GENE POLYMORPHISMS; INNATE IMMUNITY;

D O I：

10.1007/s00281-009-0152-9

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Alcoholic liver disease and nonalcoholic liver disease represent a leading cause of liver disease and share similar pathogenic mechanisms among which activation of the immune system plays a key role. The main events consist in (a) activation of Kupffer cells via TLR-4 by LPS and fatty acids (b) complement activation (c) increased release of proinflammatory mediators (d) alteration in NK and NKT cell number/activity (e) activation of the adaptive immune system. At the same time, activation of intracellular pro-inflammatory pathways by cytokines and bacterial products, inhibit insulin signaling favoring lipogenesis, metabolic alterations, and cell damage.

引用

页码：359 / 369

页数：11

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