Murine hepatic stellate cells veto CD8 T cell activation by a CD54‐dependent mechanism

Frank A. Schildberg, Alexandra Wojtalla, Sören V. Siegmund, Elmar Endl, Linda Diehl, Zeinab Abdullah, Christian Kurts, Percy A. Knolle – 12 April 2011 – The liver has a role in T cell tolerance induction, which is mainly achieved through the functions of tolerogenic hepatic antigen‐presenting cells (APCs) and regulatory T cells. Hepatic stellate cells (HSCs) are known to have various immune functions, which range from immunogenic antigen presentation to the induction of T cell apoptosis. Here we report a novel role for stellate cells in vetoing the priming of naive CD8 T cells.

Serum and liver iron differently regulate the bone morphogenetic protein 6 (BMP6)‐SMAD signaling pathway in mice

Elena Corradini, Delphine Meynard, Qifang Wu, Shan Chen, Paolo Ventura, Antonello Pietrangelo, Jodie L. Babitt – 12 April 2011 – The bone morphogenetic protein 6 (BMP6)‐SMAD signaling pathway is a central regulator of hepcidin expression and systemic iron balance. However, the molecular mechanisms by which iron is sensed to regulate BMP6‐SMAD signaling and hepcidin expression are unknown. Here we examined the effects of circulating and tissue iron on Bmp6‐Smad pathway activation and hepcidin expression in vivo after acute and chronic enteral iron administration in mice.

Antiviral activity of the hepatitis C virus polymerase inhibitor filibuvir in genotype 1–infected patients

Frank Wagner, Robert Thompson, Constantino Kantaridis, Paul Simpson, Philip J. F. Troke, Shyla Jagannatha, Srividya Neelakantan, Vivek S. Purohit, Jennifer L. Hammond – 12 April 2011 – More effective and better‐tolerated therapies are needed for chronic hepatitis C virus (HCV) infection. Among the direct‐acting anti‐HCV agents in development is the nonstructural 5B protein (NS5B polymerase) non‐nucleoside inhibitor filibuvir.

Fatty acid and endotoxin activate inflammasomes in mouse hepatocytes that release danger signals to stimulate immune cells

Timea Csak, Michal Ganz, Justin Pespisa, Karen Kodys, Angela Dolganiuc, Gyongyi Szabo – 12 April 2011 – The pathogenesis of nonalcoholic steatohepatitis (NASH) and inflammasome activation involves sequential hits. The inflammasome, which cleaves pro–interleukin‐1β (pro–IL‐1β) into secreted IL‐1β, is induced by endogenous and exogenous danger signals. Lipopolysaccharide (LPS), a toll‐like receptor 4 ligand, plays a role in NASH and also activates the inflammasome.

The metastasis‐associated protein‐1 gene encodes a host permissive factor for schistosomiasis, a leading global cause of inflammation and cancer

Sujit S. Nair, Anitha Bommana, Jeffrey M. Bethony, Amanda J. Lyon, Kazufumi Ohshiro, Suresh B. Pakala, Gabriel Rinaldi, Brian Keegan, Sutas Suttiprapa, Maria V. Periago, Peter J. Hotez, Paul J. Brindley, Rakesh Kumar – 12 April 2011 – Schistosoma haematobium is responsible for two‐thirds of the world's 200 million to 400 million cases of human schistosomiasis. It is a group 1 carcinogen and a leading cause of bladder cancer that occurs after years of chronic inflammation, fibrosis, and hyperproliferation in the host liver.

Apoptosis signal‐regulating kinase 1 inhibits hepatocarcinogenesis by controlling the tumor‐suppressing function of stress‐activated mitogen‐activated protein kinase

Hayato Nakagawa, Yoshihiro Hirata, Kohsuke Takeda, Yoku Hayakawa, Takehiro Sato, Hiroto Kinoshita, Kei Sakamoto, Wachiko Nakata, Yohko Hikiba, Masao Omata, Haruhiko Yoshida, Kazuhiko Koike, Hidenori Ichijo, Shin Maeda – 12 April 2011 – The stress‐activated mitogen‐activated protein kinases (MAPKs), c‐Jun NH2‐terminal kinase (JNK), and p38 have been implicated in hepatocarcinogenesis. Although the many interrelated functions of JNK and p38 are precisely regulated by upstream signaling molecules, little is known about upstream regulators.

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