Jacquelyn J. Maher
J Clin Invest.
2009;
119(2):246–249
doi:10.1172/JCI38178
This article Copyright © 2009, The American Society for Clinical Investigation
Abstract
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T
he 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.
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