Christiane Wiegard, Christian Frenzel, Johannes Herkel, Karl‐Josef Kallen, Edgar Schmitt, Ansgar W. Lohse – 16 June 2005 – CD4+CD25+ regulatory T cells (Treg) are important mediators of peripheral immune tolerance; however, whether Treg participate also in hepatic immune tolerance is not clear. Therefore, we tested the potential of Treg to suppress stimulation of CD4+ T cells by liver sinusoidal endothelial cells (LSEC), Kupffer cells (KC), or hepatocytes.

Kerstin Herzer, Tom M. Ganten, Henning Schulze‐Bergkamen, Anne Grosse‐Wilde, Ronald Koschny, Peter H. Krammer, Henning Walczak – 16 June 2005 – Transforming growth factor β (TGF‐β) has been shown to induce apoptotic cell death in normal and transformed hepatocytes. However, the exact mechanism through which TGF‐β induces cell death is still unknown. We examined a potential role of various death receptor/ligand systems in TGF‐β–induced apoptosis and identified the tumor necrosis factor–related apoptosis‐inducing ligand (TRAIL) as a mediator of TGF‐β–induced apoptosis in hepatoma cells.

Marco Senzolo, Evangelos Cholongitas, David Patch, Andrew Kenneth Burroughs – 16 June 2005

Andrea L. Cox, Timothy Mosbruger, Georg M. Lauer, Drew Pardoll, David L. Thomas, Stuart C. Ray – 16 June 2005 – We comprehensively studied the cellular immune response during acute human hepatitis C virus (HCV) infection by monthly prospective sampling of persons at high risk of infection. In 19 of 23 subjects, interferon‐gamma–secreting T cells specific for 1 or more peptides spanning the entire HCV polyprotein were detected 1 to 3 months after infection.

Meike Hass, Charles Hannoun, Tatyana Kalinina, Gunhild Sommer, Christoph Manegold, Stephan Günther – 16 June 2005 – The biological properties of latent or occult hepatitis B virus (HBV) have been poorly characterized as a result of the extremely low virus concentration. This report describes the phenotype of HBV reactivating in two patients after an HBsAg‐negative latency period. One patient had latent HBV infection for at least 12 years without detectable viremia and symptoms of liver disease.

16 June 2005

Morris Sherman – 16 June 2005

Harvey J. Alter – 16 June 2005

Rafael Bañares, Oscar Núñez – 16 June 2005

Brian D. Juran, Konstantinos N. Lazaridis – 16 June 2005 – Cholesterol gallstone disease is characterized by several events, including cholesterol precipitation in bile, increased bile salt hydrophobicity and gallbladder inflammation. Here, we describe the same phenotype in mice lacking the bile acid receptor, FXR. Furthermore, in susceptible wild‐type mice that recapitulate human cholesterol gallstone disease, treatment with a synthetic FXR agonist prevented sequelae of the disease.