DAMPs ramp up drug toxicity

被引：58

作者：

Maher, Jacquelyn J. ^{[1
,2
]}

机构：

[1] Univ Calif San Francisco, Dept Med, San Francisco, CA USA

[2] Univ Calif San Francisco, Ctr Liver, San Francisco, CA 94143 USA

来源：

JOURNAL OF CLINICAL INVESTIGATION | 2009年 / 119卷 / 02期

关键词：

INNATE IMMUNE-RESPONSE; ACETAMINOPHEN HEPATOTOXICITY; NALP3; INFLAMMASOME; DYING CELLS; DNA; ACTIVATION; HMGB1; INVOLVEMENT; TRIGGERS; PROTEIN;

D O I：

10.1172/JCI38178

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

The clinical syndrome of acetaminophen-induced liver injury represents the combined result of drug toxicity and a potent innate immune response that follows drug-induced cell death. In this issue of the JCI, Imaeda and colleagues report that DNA released from dying hepatocytes is a key stimulus of innate immune activation in the acetaminophen-treated mouse liver (see the related article beginning on page 305). They present evidence indicating that hepatocyte DNA promotes immune activation by acting as a danger-associated molecular pattern (DAMP) that stimulates cytokine production in neighboring sinusoidal endothelial cells via Tlr9 and the Nalp3 inflammasome.

引用

页码：246 / 249

页数：4

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