This work was supported by the intramural program of NIAAA, NIH. No conflicts of interest exist for either author.
Innate immunity and alcoholic liver fibrosis
Article first published online: 12 MAR 2008
© 2007 The Authors
Journal of Gastroenterology and Hepatology
Special Issue: 2nd International Symposium on Alcoholic Liver and Pancreatic Diseases and Cirrhosis, Kobe, Japan
Volume 23, Issue Supplement s1, pages S112–S118, March 2008
How to Cite
Jeong, W.-I. and Gao, B. (2008), Innate immunity and alcoholic liver fibrosis. Journal of Gastroenterology and Hepatology, 23: S112–S118. doi: 10.1111/j.1440-1746.2007.05274.x
- Issue published online: 12 MAR 2008
- Article first published online: 12 MAR 2008
- Accepted for publication 7 November 2007.
- hepatic stellate cell;
- innate immunity;
- liver fibrosis;
- natural killer cell
The hepatic innate immune system consists of predominant innate immunity, which plays an important role in innate defense against infection and tumor transformation. Emerging evidence suggests that innate immunity also contributes to liver injury, repair, and fibrosis. The present review summarizes the recent findings on the role of innate immunity in liver fibrosis. In general, Kupffer cells stimulate liver fibrosis via production of reactive oxygen species and pro-inflammatory cytokines, whereas natural killer (NK) cells inhibit liver fibrosis by directly killing activated hepatic stellate cells and production of γ-interferon (IFN-γ). Complement components, interferons, and Toll-like receptors have also been shown to regulate liver fibrosis. Recent evidence also suggests that modulation of innate immunity by alcohol plays an important role in the pathogenesis of alcoholic liver fibrosis. These include alcohol amplification of the profibrotic effects of Kupffer cells and suppression of the antifibrotic effects of NK/IFN-γ.