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HepatoMetaboPath SIGNED

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

Total Cost €

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EC-Contrib. €

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Partnership

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 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.

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

Project "HepatoMetaboPath" data sheet

The following table provides information about the project.

Coordinator
HELMHOLTZ ZENTRUM MUENCHEN DEUTSCHES FORSCHUNGSZENTRUM FUER GESUNDHEIT UND UMWELT GMBH 

Organization address
address: INGOLSTADTER LANDSTRASSE 1
city: NEUHERBERG
postcode: 85764
website: www.helmholtz-muenchen.de

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

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    HELMHOLTZ ZENTRUM MUENCHEN DEUTSCHES FORSCHUNGSZENTRUM FUER GESUNDHEIT UND UMWELT GMBH DE (NEUHERBERG) coordinator 1˙995˙860.00

Map

 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.

 Publications

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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