Nature Communications (Apr 2020)
The platelet receptor CLEC-2 blocks neutrophil mediated hepatic recovery in acetaminophen induced acute liver failure
- 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
Affiliations
- Abhishek Chauhan
- Centre 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 Birmingham
- Lozan Sheriff
- Centre 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 Birmingham
- Mohammed T. Hussain
- Centre 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 Birmingham
- Gwilym J. Webb
- Centre 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 Birmingham
- Daniel A. Patten
- Centre 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 Birmingham
- Emma L. Shepherd
- Centre 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 Birmingham
- Robert Shaw
- Technology Hub, College of Medical and Dental Sciences, University of Birmingham
- Christopher J. Weston
- Centre 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 Birmingham
- Debashis Haldar
- Centre 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 Birmingham
- Samuel Bourke
- Centre 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 Birmingham
- Rajan Bhandari
- Centre 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 Birmingham
- Stephanie Watson
- Institute of Cardiovascular Sciences, The Medical School, University of Birmingham
- David H. Adams
- Centre 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 Birmingham
- Steve P. Watson
- Institute of Cardiovascular Sciences, The Medical School, University of Birmingham
- Patricia F. Lalor
- Centre 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 Birmingham
- DOI
- https://doi.org/10.1038/s41467-020-15584-3
- Journal volume & issue
-
Vol. 11,
no. 1
pp. 1 – 12
Abstract
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.
