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.

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.

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).

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.

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