The interplay of type I and type II interferons in murine autoimmune cholangitis as a basis for sex‐biased autoimmunity

Heekyong R. Bae, Deborah L. Hodge, Guo‐Xiang Yang, Patrick S.C. Leung, Sathi Babu Chodisetti, Julio C. Valencia, Michael Sanford, John M. Fenimore, Ziaur S.M. Rahman, Koichi Tsuneyama, Gary L. Norman, M. Eric Gershwin, Howard A. Young – 16 September 2017 – We have reported on a murine model of autoimmune cholangitis, generated by altering the AU‐rich element (ARE) by deletion of the interferon gamma (IFN‐γ) 3' untranslated region (coined ARE‐Del−/−), that has striking similarities to human primary biliary cholangitis (PBC) with female predominance.

Graft‐infiltrating PD‐L1hi cross‐dressed dendritic cells regulate antidonor T cell responses in mouse liver transplant tolerance

Yoshihiro Ono, Angelica Perez‐Gutierrez, Toshimasa Nakao, Helong Dai, Geoffrey Camirand, Osamu Yoshida, Shinichiro Yokota, Donna Beer Stolz, Mark A. Ross, Adrian E. Morelli, David A. Geller, Angus W. Thomson – 16 September 2017 – Although a key role of cross‐dressing has been established in immunity to viral infection and more recently in the instigation of transplant rejection, its role in tolerance is unclear.

Validation of artificial neural networks as a methodology for donor‐recipient matching for liver transplantation

María Dolores Ayllón, Rubén Ciria, Manuel Cruz‐Ramírez, María Pérez‐Ortiz, Irene Gómez, Roberto Valente, John O'Grady, Manuel de la Mata, César Hervás‐Martínez, Nigel D. Heaton, Javier Briceño – 16 September 2017 – In 2014, we reported a model for donor‐recipient (D‐R) matching in liver transplantation (LT) based on artificial neural networks (ANNs) from a Spanish multicenter study (Model for Allocation of Donor and Recipient in España [MADR‐E]). The aim is to test the ANN‐based methodology in a different European health care system in order to validate it.

Induction of cancer cell stemness by depletion of macrohistone H2A1 in hepatocellular carcinoma

Oriana Lo Re, Caterina Fusilli, Francesca Rappa, Matthias Van Haele, Julien Douet, Jana Pindjakova, Sura Wanessa Rocha, Illar Pata, Barbora Valčíková, Stjepan Uldrijan, Raymond S. Yeung, Christina Alves Peixoto, Tania Roskams, Marcus Buschbeck, Tommaso Mazza, Manlio Vinciguerra – 15 September 2017 – Hepatocellular carcinomas (HCC) contain a subpopulation of cancer stem cells (CSCs), which exhibit stem cell–like features and are responsible for tumor relapse, metastasis, and chemoresistance.

LiverLearning®: 2017 Webinar: Chronic Hepatitis B and Pregnancy: Management and Prevention of Vertical Transmission

The management of women of child-bearing age and pregnant women with chronic hepatitis B requires special consideration due to the potential effects of antiviral therapy on unborn fetus and potential for hepatitis flares for pregnant and postpartum women. While universal maternal screening programs and immunoprophylaxis to newborns have greatly reduced mother-to-child-transmission (MTCT), immunoprophylaxis can fail in up to 30% of infants, especially in mothers with high HBV DNA levels and positive HBeAg.

Reassessing the safety concerns of utilizing blood donations from patients with hemochromatosis

Adam C. Winters, Douglas Tremblay, Suzanne Arinsburg, John Mascarenhas, Thomas D. Schiano – 13 September 2017 – Hereditary hemochromatosis (HH) is a genetic disorder of iron metabolism that may lead to iron overload. Clinical penetrance is low, however those afflicted may develop cirrhosis, hepatocellular carcinoma, diabetes mellitus, and cardiomyopathy. Treatment of HH involves regular phlebotomy to reduce the systemic iron burden.

NLRP3 inflammasome driven liver injury and fibrosis: Roles of IL‐17 and TNF in mice

Alexander Wree, Matthew D. McGeough, Maria Eugenia Inzaugarat, Akiko Eguchi, Susanne Schuster, Casey D. Johnson, Carla A. Peña, Lukas J. Geisler, Bettina G. Papouchado, Hal M. Hoffman, Ariel E. Feldstein – 13 September 2017 – The NLRP3 inflammasome, a caspase‐1 activation platform, plays a key role in the modulation of liver inflammation and fibrosis. Here, we tested the hypothesis that interleukin 17 (IL‐17) and tumor necrosis factor (TNF) are key cytokines involved in amplifying and perpetuating the liver damage and fibrosis resulting from NLRP3 activation.

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