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Roles of Liver Innate Immune Cells in Nonalcoholic Fatty Liver Disease

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Specialty Gastroenterology
Date 2010 Sep 28
PMID 20872965
Citations 49
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Abstract

Nonalcoholic fatty liver disease (NAFLD) has become the most common liver disease in the United States and other developed countries and is expected to increase in the next few years. Emerging data suggest that some patients with NAFLD may progress to nonalcoholic steatohepatitis (NASH), cirrhosis and even hepatocellular carcinoma. NAFLD can also promote the development and progression of disease in other organ systems, such as the cardiovascular and endocrine (i.e. diabetes) systems. Thus, understanding the pathogenesis of NAFLD is of great clinical importance and is critical for the prevention and treatment of the disease. Although the "two-hit hypothesis" is generally accepted, the exact pathogenesis of NAFLD has not been clearly established. The liver is an important innate immune organ with large numbers of innate immune cells, including Kupffer cells (KCs), natural killer T (NKT) cells and natural killer (NK) cells. Recent data show that an imbalance in liver cytokines may be implicated in the development of fatty liver disease. For example, Th1 cytokine excess may be a common pathogenic mechanism for hepatic insulin resistance and NASH. Innate immune cells in the liver play important roles in the excessive production of hepatic Th1 cytokines in NAFLD. In addition, liver innate immune cells participate in the pathogenesis of NAFLD in other ways. For example, activated KCs can generate reactive oxygen species, which induce liver injury. This review will focus primarily on the possible effect and mechanism of KCs, NKT cells and NK cells in the development of NAFLD.

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References
1.
Wei Y, Clark S, Morris E, Thyfault J, Uptergrove G, Whaley-Connell A . Angiotensin II-induced non-alcoholic fatty liver disease is mediated by oxidative stress in transgenic TG(mRen2)27(Ren2) rats. J Hepatol. 2008; 49(3):417-28. PMC: 2683586. DOI: 10.1016/j.jhep.2008.03.018. View

2.
Van Hoek B . Non-alcoholic fatty liver disease: a brief review. Scand J Gastroenterol Suppl. 2005; (241):56-9. DOI: 10.1080/00855920410011013. View

3.
Maher J, Leon P, Ryan J . Beyond insulin resistance: Innate immunity in nonalcoholic steatohepatitis. Hepatology. 2008; 48(2):670-8. PMC: 3592568. DOI: 10.1002/hep.22399. View

4.
Doherty D, OFarrelly C . Innate and adaptive lymphoid cells in the human liver. Immunol Rev. 2000; 174:5-20. DOI: 10.1034/j.1600-0528.2002.017416.x. View

5.
Lamas O, Martinez J, Marti A . Energy restriction restores the impaired immune response in overweight (cafeteria) rats. J Nutr Biochem. 2004; 15(7):418-25. DOI: 10.1016/j.jnutbio.2004.02.003. View