The platelet receptor CLEC-2 blocks neutrophil mediated hepatic recovery in acetaminophen induced acute liver failure

The molecular mechanisms that drive irreversible acute liver failure remain poorly characterized. Here, the authors show that the recently discovered platelet receptor CLEC-2 (C-type lectin-like receptor) perpetuates and worsens liver damage during acute liver injury by blocking restorative neutroph...

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Main Authors: Abhishek Chauhan, Lozan Sheriff, Mohammed T. Hussain, Gwilym J. Webb, Daniel A. Patten, Emma L. Shepherd, Robert Shaw, Christopher J. Weston, Debashis Haldar, Samuel Bourke, Rajan Bhandari, Stephanie Watson, David H. Adams, Steve P. Watson, Patricia F. Lalor
Format: Article
Language:English
Published: Nature Publishing Group 2020-04-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-020-15584-3
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spelling doaj-a6f8dbdcb34b42c0a82ada447cf8eac92021-05-11T08:31:13ZengNature Publishing GroupNature Communications2041-17232020-04-0111111210.1038/s41467-020-15584-3The platelet receptor CLEC-2 blocks neutrophil mediated hepatic recovery in acetaminophen induced acute liver failureAbhishek Chauhan0Lozan Sheriff1Mohammed T. Hussain2Gwilym J. Webb3Daniel A. Patten4Emma L. Shepherd5Robert Shaw6Christopher J. Weston7Debashis Haldar8Samuel Bourke9Rajan Bhandari10Stephanie Watson11David H. Adams12Steve P. Watson13Patricia F. Lalor14Centre for Liver and Gastrointestinal Research, Institute of Immunology and Inflammation, and National Institute for Health Research (NIHR) Birmingham Biomedical Research Centre, The Medical School, University of BirminghamCentre for Liver and Gastrointestinal Research, Institute of Immunology and Inflammation, and National Institute for Health Research (NIHR) Birmingham Biomedical Research Centre, The Medical School, University of BirminghamCentre for Liver and Gastrointestinal Research, Institute of Immunology and Inflammation, and National Institute for Health Research (NIHR) Birmingham Biomedical Research Centre, The Medical School, University of BirminghamCentre for Liver and Gastrointestinal Research, Institute of Immunology and Inflammation, and National Institute for Health Research (NIHR) Birmingham Biomedical Research Centre, The Medical School, University of BirminghamCentre for Liver and Gastrointestinal Research, Institute of Immunology and Inflammation, and National Institute for Health Research (NIHR) Birmingham Biomedical Research Centre, The Medical School, University of BirminghamCentre for Liver and Gastrointestinal Research, Institute of Immunology and Inflammation, and National Institute for Health Research (NIHR) Birmingham Biomedical Research Centre, The Medical School, University of BirminghamTechnology Hub, College of Medical and Dental Sciences, University of BirminghamCentre for Liver and Gastrointestinal Research, Institute of Immunology and Inflammation, and National Institute for Health Research (NIHR) Birmingham Biomedical Research Centre, The Medical School, University of BirminghamCentre for Liver and Gastrointestinal Research, Institute of Immunology and Inflammation, and National Institute for Health Research (NIHR) Birmingham Biomedical Research Centre, The Medical School, University of BirminghamCentre for Liver and Gastrointestinal Research, Institute of Immunology and Inflammation, and National Institute for Health Research (NIHR) Birmingham Biomedical Research Centre, The Medical School, University of BirminghamCentre for Liver and Gastrointestinal Research, Institute of Immunology and Inflammation, and National Institute for Health Research (NIHR) Birmingham Biomedical Research Centre, The Medical School, University of BirminghamInstitute of Cardiovascular Sciences, The Medical School, University of BirminghamCentre for Liver and Gastrointestinal Research, Institute of Immunology and Inflammation, and National Institute for Health Research (NIHR) Birmingham Biomedical Research Centre, The Medical School, University of BirminghamInstitute of Cardiovascular Sciences, The Medical School, University of BirminghamCentre for Liver and Gastrointestinal Research, Institute of Immunology and Inflammation, and National Institute for Health Research (NIHR) Birmingham Biomedical Research Centre, The Medical School, University of BirminghamThe molecular mechanisms that drive irreversible acute liver failure remain poorly characterized. Here, the authors show that the recently discovered platelet receptor CLEC-2 (C-type lectin-like receptor) perpetuates and worsens liver damage during acute liver injury by blocking restorative neutrophil driven inflammation.https://doi.org/10.1038/s41467-020-15584-3
collection DOAJ
language English
format Article
sources DOAJ
author Abhishek Chauhan
Lozan Sheriff
Mohammed T. Hussain
Gwilym J. Webb
Daniel A. Patten
Emma L. Shepherd
Robert Shaw
Christopher J. Weston
Debashis Haldar
Samuel Bourke
Rajan Bhandari
Stephanie Watson
David H. Adams
Steve P. Watson
Patricia F. Lalor
spellingShingle Abhishek Chauhan
Lozan Sheriff
Mohammed T. Hussain
Gwilym J. Webb
Daniel A. Patten
Emma L. Shepherd
Robert Shaw
Christopher J. Weston
Debashis Haldar
Samuel Bourke
Rajan Bhandari
Stephanie Watson
David H. Adams
Steve P. Watson
Patricia F. Lalor
The platelet receptor CLEC-2 blocks neutrophil mediated hepatic recovery in acetaminophen induced acute liver failure
Nature Communications
author_facet Abhishek Chauhan
Lozan Sheriff
Mohammed T. Hussain
Gwilym J. Webb
Daniel A. Patten
Emma L. Shepherd
Robert Shaw
Christopher J. Weston
Debashis Haldar
Samuel Bourke
Rajan Bhandari
Stephanie Watson
David H. Adams
Steve P. Watson
Patricia F. Lalor
author_sort Abhishek Chauhan
title The platelet receptor CLEC-2 blocks neutrophil mediated hepatic recovery in acetaminophen induced acute liver failure
title_short The platelet receptor CLEC-2 blocks neutrophil mediated hepatic recovery in acetaminophen induced acute liver failure
title_full The platelet receptor CLEC-2 blocks neutrophil mediated hepatic recovery in acetaminophen induced acute liver failure
title_fullStr The platelet receptor CLEC-2 blocks neutrophil mediated hepatic recovery in acetaminophen induced acute liver failure
title_full_unstemmed The platelet receptor CLEC-2 blocks neutrophil mediated hepatic recovery in acetaminophen induced acute liver failure
title_sort platelet receptor clec-2 blocks neutrophil mediated hepatic recovery in acetaminophen induced acute liver failure
publisher Nature Publishing Group
series Nature Communications
issn 2041-1723
publishDate 2020-04-01
description The molecular mechanisms that drive irreversible acute liver failure remain poorly characterized. Here, the authors show that the recently discovered platelet receptor CLEC-2 (C-type lectin-like receptor) perpetuates and worsens liver damage during acute liver injury by blocking restorative neutrophil driven inflammation.
url https://doi.org/10.1038/s41467-020-15584-3
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