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HepatoMetaboPath SIGNED

Cellular and molecular mechanisms of metabolic immune activation triggering non-alcoholic steatohepatitis (NASH) and HCC

Total Cost €


EC-Contrib. €






 HepatoMetaboPath project word cloud

Explore the words cloud of the HepatoMetaboPath project. It provides you a very rough idea of what is the project "HepatoMetaboPath" about.

significantly    metabolic    recognition    priming    former    cells    frequent    diseases    model    hepatocyte    expertise    overweight    danger    found    nash    carcinoma    dimensions    clinically    determinants    cd8t    clinical    steatohepatitis    normalization    fibrosis    lacking    cell    unknown    talk    mouse    therapies    syndrome    nkt    immune    transition    first    underlining    underlying    inflammation    pandemic    industrialized    world    rising    countries    activation    subsequent    trend    demonstrated    natural    causing    hepatocellular    poorly    genetic    fatty    activated    lipid    context    hepatic    patients    pathology    death    cancer    pathogen    molecular    nafld    types    metabolism    reaching    disease    viruses    relevance    human    antigen    time    hcc    patterns    mechanisms    recapitulating    alcoholic    efficacious    profile    environmental    killer    crosstalk    group    hepatocytes    usa    manifest    reduce    suffices    cross    identical    hepatitis    liver    alter    cd8   

Project "HepatoMetaboPath" data sheet

The following table provides information about the project.


Organization address
postcode: 85764

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Germany [DE]
 Total cost 1˙995˙860 €
 EC max contribution 1˙995˙860 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2015-CoG
 Funding Scheme ERC-COG
 Starting year 2016
 Duration (year-month-day) from 2016-07-01   to  2021-06-30


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 


 Project objective

Overweight and metabolic syndrome are reaching pandemic dimensions in industrialized countries and are rising in developing countries. Clinically these diseases can manifest in non-alcoholic fatty liver disease (NAFLD), the most frequent liver disease world-wide. A significant number of NAFLD patients develop non-alcoholic steatohepatitis (NASH), fibrosis and hepatocellular carcinoma (HCC), making NASH-driven HCC the most rapidly increasing cancer in the USA, with a similar trend in Europe. While HCC is the second most common cause of cancer related death, the mechanisms triggering NASH and subsequent HCC are poorly understood and efficacious therapies are lacking. My group has strong expertise in inflammation-driven HCC (e.g. by Hepatitis B, C viruses). Recently, we have established a mouse model of NASH-driven HCC recapitulating human pathology in the context of metabolic syndrome. We demonstrated for the first time that CD8 T- and natural killer T (NKT)-cells become activated during metabolic syndrome, cross-talk with hepatocytes and alter hepatic lipid metabolism causing NASH and HCC. We found an identical profile of CD8T and NKT-cell activation in human NASH underlining the clinical relevance of our model. As the mechanisms of immune cell activation in NASH and transition to HCC remain unknown, this research proposal aims to (1) Identify the priming cell types in metabolic CD8 T-, NKT-cell activation and the molecular mechanisms of immune cell-hepatocyte crosstalk. (2) Determine the role of antigen recognition and danger- or pathogen-associated molecular patterns in NASH/HCC. (3) Identify the environmental and genetic determinants of NASH to HCC transition. Our findings will enhance the understanding of NASH and HCC development by identifying the underlying mechanisms of immune cell activation. We will identify genetic changes facilitating NASH to HCC transition and whether metabolic normalization of former NASH patients suffices to significantly reduce HCC.


year authors and title journal last update
List of publications.
2018 Anna Lorentzen, Paul F. Becker, Jan Kosla, Massimo Saini, Kathrin Weidele, Paolo Ronchi, Corinna Klein, Monika J. Wolf, Felix Geist, Bastian Seubert, Marc Ringelhan, Daniela Mihic-Probst, Knud Esser, Marko Roblek, Felix Kuehne, Gaia Bianco, Tracy O’Connor, Quentin Müller, Kathleen Schuck, Sebastian Lange, Daniel Hartmann, Saskia Spaich, Olaf Groß, Jochen Utikal, Sebastian Haferkamp, Martin R.
Single cell polarity in liquid phase facilitates tumour metastasis
published pages: , ISSN: 2041-1723, DOI: 10.1038/s41467-018-03139-6
Nature Communications 9/1 2019-09-02
2019 Quentin M. Anstee, Helen L. Reeves, Elena Kotsiliti, Olivier Govaere, Mathias Heikenwalder
From NASH to HCC: current concepts and future challenges
published pages: 411-428, ISSN: 1759-5045, DOI: 10.1038/s41575-019-0145-7
Nature Reviews Gastroenterology & Hepatology 16/7 2019-09-02
2018 Marc Ringelhan, Dominik Pfister, Tracy O’Connor, Eli Pikarsky, Mathias Heikenwalder
The immunology of hepatocellular carcinoma
published pages: 222-232, ISSN: 1529-2908, DOI: 10.1038/s41590-018-0044-z
Nature Immunology 19/3 2019-09-02

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