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International Journal of Endocrinology
Volume 2013 (2013), Article ID 972962, 12 pages
Research Article

Major Histocompatibility Class II Pathway Is Not Required for the Development of Nonalcoholic Fatty Liver Disease in Mice

1Department of Physiology, University of Lausanne, Rue du Bugnon 7, 1005 Lausanne, Switzerland
2Center for Integrative Genomics, University of Lausanne, 1010 Lausanne, Switzerland
3Nestlé Research Center, Vers-chez-les-Blanc, 1000 Lausanne 26, Switzerland

Received 12 February 2013; Accepted 22 March 2013

Academic Editor: Jun Ding

Copyright © 2013 Gilles Willemin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Single-nucleotide polymorphisms within major histocompatibility class II (MHC II) genes have been associated with an increased risk of drug-induced liver injury. However, it has never been addressed whether the MHC II pathway plays an important role in the development of nonalcoholic fatty liver disease, the most common form of liver disease. We used a mouse model that has a complete knockdown of genes in the MHC II pathway (MHCIIΔ/Δ). Firstly we studied the effect of high-fat diet-induced hepatic inflammation in these mice. Secondly we studied the development of carbon-tetra-chloride- (CCl4-) induced hepatic cirrhosis. After the high-fat diet, both groups developed obesity and hepatic steatosis with a similar degree of hepatic inflammation, suggesting no impact of the knockdown of MHC II on high-fat diet-induced inflammation in mice. In the second study, we confirmed that the CCl4 injection significantly upregulated the MHC II genes in wild-type mice. The CCl4 treatment significantly induced genes related to the fibrosis formation in wild-type mice, whereas this was lower in MHCIIΔ/Δ mice. The liver histology, however, showed no detectable difference between groups, suggesting that the MHC II pathway is not required for the development of hepatic fibrosis induced by CCl4.