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. Author manuscript; available in PMC: 2012 May 1.
Published in final edited form as: Alcohol Clin Exp Res. 2011 Feb 1;35(5):787–793. doi: 10.1111/j.1530-0277.2010.01399.x

Fig. 1. Molecular mechanisms of alcoholic liver disease (ALD): roles of innate immunity and cytokines.

Fig. 1

Chronic alcohol exposure leads to innate immunity activation such as Kupffer cells and LPS/TLR4. Activated Kupffer cells produce TNF-α and toxins that contribute to ALD. LPS also stimulates Kupffer cells to produce hepatoprotective cytokines (such as IL-6) and anti-inflammatory cytokines (such as IL-10). Both IL-6 and IL-10 play protective roles in ameliorating ALD via activation of STAT3 in different types of liver cells. Alcohol consumption inhibits IL-6 activation of STAT3 in hepatocytes and sinusoidal endothelial cells, and inhibits IL-10 activation of STAT3 in monocytes, contributing to the pathogenesis of ALD. Alcohol consumption also suppresses some other components of innate immunity such as NK cells. NK cells play important roles in anti-viral, anti-tumor, and anti-fibrotic defenses in the liver. Alcohol inhibits NK cell functions via multiple mechanisms as described in the text, contributing to the pathogenesis of ALD.