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Liver cirrhosis is a leading cause of mortality in Western countries and the major risk factor for the development of hepatocellular carcinoma, a difficult to treat malignancy with a poor prognosis. In recent years, the management of cirrhotic patients has considerably improved due to better ability to deal with complications such as portal hypertensive bleeding, hepatorenal syndrome and hepatocellular carcinoma. Unless the causal agent is removed, no therapies are currently available to slow down the progressive worsening of hepatic function after the development of cirrhosis, and liver transplantation remains the only approach that has an impact in the long term. Considerable advancements have also been made in the understanding of the pathophysiology of hepatic fibrosis, and the pivotal role played by hepatic inflammation has been clearly defined. Inflammation is part of the tissue ‘wound healing’ response, and leucocyte populations differentially modulate the process of fibrogenesis, that leads to the development of cirrhosis.1 Monocytes and activated macrophages contribute to the development and progression of fibrosis via expression of numerous cytokines, such as platelet-derived growth factor and transforming growth factor-β1, or generation of reactive oxygen intermediates. The role of T cells is more complex, and the available data indicate that a Th1-polarised response is associated with reduced deposition of extracellular matrix, partly mediated by secretion of interferon (IFN)-γ, whereas Th2-related cytokines such as interleukin (IL)-4 and IL-13 cause a more rapid progression of fibrosis.1 Once cirrhosis has been established, the presence of inflammation and the related hyperproduction of cytokines, including tumour necrosis factor (TNF)-α, in the splanchnic district and in the systemic circulation, is responsible for the worsening of portal hypertension and appearance of hyperdynamic circulation.2 …