Extracellular vesicles in liver pathobiology: Small particles with big impact

Petra Hirsova, Samar H. Ibrahim, Vikas K. Verma, Leslie A. Morton, Vijay H. Shah, Nicholas F. LaRusso, Gregory J. Gores, Harmeet Malhi – 15 September 2016 – Extracellular vesicles (EVs) are nanometer‐sized, membrane‐bound vesicles released by cells into the extracellular milieu. EVs are now recognized to play a critical role in cell‐to‐cell communication. EVs contain important cargo in the form of proteins, lipids, and nucleic acids and serve as vectors for delivering this cargo from donor to acceptor or target cell.

The cystic fibrosis transmembrane conductance regulator controls biliary epithelial inflammation and permeability by regulating Src tyrosine kinase activity

Romina Fiorotto, Ambra Villani, Antonis Kourtidis, Roberto Scirpo, Mariangela Amenduni, Peter J. Geibel, Massimiliano Cadamuro, Carlo Spirli, Panos Z. Anastasiadis, Mario Strazzabosco – 15 September 2016 – In the liver, the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) regulates bile secretion and other functions at the apical membrane of biliary epithelial cells (i.e., cholangiocytes). CF‐related liver disease is a major cause of death in patients with CF.

Characterization of the Specificity, Functionality, and Durability of Host T‐Cell Responses Against the Full‐Length Hepatitis E Virus

Anthony Brown, John S. Halliday, Leo Swadling, Richie G. Madden, Richard Bendall, Jeremy G. Hunter, James Maggs, Peter Simmonds, Donald B. Smith, Louisa Vine, Cara McLaughlin, Jane Collier, David Bonsall, Katie Jeffery, Susanna Dunachie, Paul Klenerman, Jacques Izopet, Nassim Kamar, Harry R. Dalton, Eleanor Barnes – 15 September 2016 – The interplay between host antiviral immunity and immunopathology during hepatitis E virus (HEV) infection determines important clinical outcomes.

IRAKM‐Mincle axis links cell death to inflammation: Pathophysiological implications for chronic alcoholic liver disease

Hao Zhou, Minjia Yu, Junjie Zhao, Bradley N. Martin, Sanjoy Roychowdhury, Megan R. McMullen, Emily Wang, Paul L. Fox, Sho Yamasaki, Laura E. Nagy, Xiaoxia Li – 15 September 2016 – Lipopolysaccharide (LPS)‐mediated activation of Toll‐like receptors (TLRs) in hepatic macrophages and injury to hepatocytes are major contributors to the pathogenesis of alcoholic liver disease. However, the mechanisms by which TLR‐dependent inflammatory responses and alcohol‐induced hepatocellular damage coordinately lead to alcoholic liver disease are not completely understood.

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