Primary biliary cirrhosis: A 2010 update Raoul Poupon  Journal of Hepatology  Volume 52, Issue 5, Pages 745-758 (May 2010) DOI: 10.1016/j.jhep.2009.11.027 Copyright © 2010 European Association for the Study of the Liver Terms and Conditions

Fig. 1 PBC results from a combination of multiple genetic and environmental factors that may affect the immune system and the liver. Journal of Hepatology 2010 52, 745-758DOI: (10.1016/j.jhep.2009.11.027) Copyright © 2010 European Association for the Study of the Liver Terms and Conditions

Fig. 2 PBC sequential events: from PDCE2-breakdown tolerance to cirrhosis and liver failure. Journal of Hepatology 2010 52, 745-758DOI: (10.1016/j.jhep.2009.11.027) Copyright © 2010 European Association for the Study of the Liver Terms and Conditions

Fig. 3 (A) Typical aspect of the lymphocytic interface hepatitis in PBC; (B) biliary piecemeal necrosis with marked increase of ductular profiles accompanied by oedema, neutrophils, and fibroplasia. Journal of Hepatology 2010 52, 745-758DOI: (10.1016/j.jhep.2009.11.027) Copyright © 2010 European Association for the Study of the Liver Terms and Conditions

Fig. 4 Schematic representation of the putative sequence events in the fibrogenesis process of PBC (ET1: endothelin 1, PDGF: platelet-derived growth factor, VEGF: vascular epithelial growth factor, CCL2: chemokine ligand 2, TGFβ: transforming growth factor β, NGF: nerve growth factor, BMD: bone marrow derived-cells, EMT: epithelial–mesenchymal transition). Journal of Hepatology 2010 52, 745-758DOI: (10.1016/j.jhep.2009.11.027) Copyright © 2010 European Association for the Study of the Liver Terms and Conditions

Fig. 5 Patterns of development of ductopenia and fibrosis in the three major clinical forms of PBC. Journal of Hepatology 2010 52, 745-758DOI: (10.1016/j.jhep.2009.11.027) Copyright © 2010 European Association for the Study of the Liver Terms and Conditions