Early changes in interferon signaling define natural killer cell response and refractoriness to interferon‐based therapy of hepatitis C patients

Birgit Edlich, Golo Ahlenstiel, Aintzane Azpiroz Zabaleta, Jonathan Stoltzfus, Mazen Noureddin, Elisavet Serti, Jordan J. Feld, T. Jake Liang, Yaron Rotman, Barbara Rehermann – 24 August 2011 – Natural killer (NK) cells exhibit a polarized phenotype with increased cytotoxicity and decreased interferon gamma (IFN‐γ) production in chronic hepatitis C virus (HCV) infection.

Dendritic cell regulation of carbon tetrachloride–induced murine liver fibrosis regression

Jingjing Jiao, David Sastre, Maria Isabel Fiel, Ursula E. Lee, Zahra Ghiassi‐Nejad, Florent Ginhoux, Eric Vivier, Scott L. Friedman, Miriam Merad, Costica Aloman – 24 August 2011 – Although hepatic fibrosis typically follows chronic inflammation, fibrosis will often regress after cessation of liver injury. In this study, we examined whether liver dendritic cells (DCs) play a role in liver fibrosis regression using carbon tetrachloride to induce liver injury. We examined DC dynamics during fibrosis regression and their capacity to modulate liver fibrosis regression upon cessation of injury.

Shedding of syndecan‐1 from human hepatocytes alters very low density lipoprotein clearance

Yiping Deng, Erin M. Foley, Jon C. Gonzales, Philip L. Gordts, Yulin Li, Jeffrey D. Esko – 24 August 2011 – We recently showed that the heparan sulfate proteoglycan syndecan‐1 mediates hepatic clearance of triglyceride‐rich lipoproteins in mice based on systemic deletion of syndecan‐1 and hepatocyte‐specific inactivation of sulfotransferases involved in heparan sulfate biosynthesis. Here, we show that syndecan‐1 expressed on primary human hepatocytes and Hep3B human hepatoma cells can mediate binding and uptake of very low density lipoprotein (VLDL).

Association of gene expression involving innate immunity and genetic variation in interleukin 28B with antiviral response

Yasuhiro Asahina, Kaoru Tsuchiya, Masaru Muraoka, Keisuke Tanaka, Yuichiro Suzuki, Nobuharu Tamaki, Yoshihide Hoshioka, Yutaka Yasui, Tomoji Katoh, Takanori Hosokawa, Ken Ueda, Hiroyuki Nakanishi, Jun Itakura, Yuka Takahashi, Masayuki Kurosaki, Nobuyuki Enomoto, Sayuri Nitta, Naoya Sakamoto, Namiki Izumi – 24 August 2011 – Innate immunity plays an important role in host antiviral response to hepatitis C viral (HCV) infection. Recently, single nucleotide polymorphisms (SNPs) of IL28B and host response to peginterferon α (PEG‐IFNα) and ribavirin (RBV) were shown to be strongly associated.

Immunoglobulin M levels inversely correlate with CD40 ligand promoter methylation in patients with primary biliary cirrhosis

Ana Lleo, Jieyue Liao, Pietro Invernizzi, Ming Zhao, Francesca Bernuzzi, Le Ma, Gaetana Lanzi, Aftab A. Ansari, Ross L. Coppel, Peng Zhang, Yijun Li, Zhiguang Zhou, Qianjin Lu, M. Eric Gershwin – 24 August 2011 – The cross‐talk of cluster of differentiation (CD)40/CD40 ligand (CD40L) plays a key role in CD4+ T‐cell priming, B‐cell terminal maturation, and immunoglobulin (Ig) class‐switch recombination. Genetic defects in the CD40L lead to a disorder characterized by elevated concentrations of serum IgM and immunodeficiency.

Higher serum testosterone is associated with increased risk of advanced hepatitis C–related liver disease in males

Donna L. White, Shariar Tavakoli‐Tabasi, Jill Kuzniarek, Rhia Pascua, David J. Ramsey, Hashem B. El‐Serag – 19 August 2011 – Males have strikingly increased risk of advanced liver disease. However, the association between testosterone and risk of hepatitis C virus (HCV)‐related advanced liver disease is unknown. We performed a cross‐sectional study in male veterans with chronic HCV. Blood samples were obtained to measure total serum testosterone and perform the FibroSURE‐ActiTest.

Determinants of spontaneous surface antigen loss in hepatitis B e antigen–negative patients with a low viral load

Tai‐Chung Tseng, Chun‐Jen Liu, Hung‐Chih Yang, Tung‐Hung Su, Chia‐Chi Wang, Chi‐Ling Chen, Stephanie Fang‐Tzu Kuo, Chen‐Hua Liu, Pei‐Jer Chen, Ding‐Shinn Chen, Jia‐Horng Kao – 19 August 2011 – Loss of hepatitis B surface antigen (HBsAg) usually indicates the cure of hepatitis B virus (HBV) infection. In spontaneous hepatitis B e antigen (HBeAg) seroconverters, lower serum HBsAg and HBV DNA levels have been shown to be associated with HBsAg loss over time. However, little is known about their impacts on HBsAg loss in HBeAg‐negative patients with limited viral replication.

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