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Infiltrating monocytes in liver injury and repair

Noninfectious liver injury causes many acute and chronic liver diseases around the globe, and particularly in developed nations. Bone marrow-derived monocytes infiltrate the damaged liver tissue and are a critical component of the innate immune response that may drive injury resolution or host death...

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Detalles Bibliográficos
Autores principales: Brempelis, Katherine J, Crispe, Ian N
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5133365/
https://www.ncbi.nlm.nih.gov/pubmed/27990288
http://dx.doi.org/10.1038/cti.2016.62
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author Brempelis, Katherine J
Crispe, Ian N
author_facet Brempelis, Katherine J
Crispe, Ian N
author_sort Brempelis, Katherine J
collection PubMed
description Noninfectious liver injury causes many acute and chronic liver diseases around the globe, and particularly in developed nations. Bone marrow-derived monocytes infiltrate the damaged liver tissue and are a critical component of the innate immune response that may drive injury resolution or host death in the short term or chronic inflammation, fibrosis and hepatocellular carcinoma in the long term. Monocytes often play dual roles in liver injury—both perpetuating inflammation and promoting resolution of inflammation and fibrosis. Thus, we will address the role that monocytes play in different experimental forms of noninfectious liver injury; considering in particular the importance of the transition from inflammatory Ly6C(hi) monocytes to pro-resolution Ly6C(lo) monocyte-derived macrophages and the consequences of this transition for disease progression and resolution.
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spelling pubmed-51333652016-12-16 Infiltrating monocytes in liver injury and repair Brempelis, Katherine J Crispe, Ian N Clin Transl Immunology Review Noninfectious liver injury causes many acute and chronic liver diseases around the globe, and particularly in developed nations. Bone marrow-derived monocytes infiltrate the damaged liver tissue and are a critical component of the innate immune response that may drive injury resolution or host death in the short term or chronic inflammation, fibrosis and hepatocellular carcinoma in the long term. Monocytes often play dual roles in liver injury—both perpetuating inflammation and promoting resolution of inflammation and fibrosis. Thus, we will address the role that monocytes play in different experimental forms of noninfectious liver injury; considering in particular the importance of the transition from inflammatory Ly6C(hi) monocytes to pro-resolution Ly6C(lo) monocyte-derived macrophages and the consequences of this transition for disease progression and resolution. Nature Publishing Group 2016-11-04 /pmc/articles/PMC5133365/ /pubmed/27990288 http://dx.doi.org/10.1038/cti.2016.62 Text en Copyright © 2016 The Author(s) http://creativecommons.org/licenses/by-nc-nd/4.0/ This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/
spellingShingle Review
Brempelis, Katherine J
Crispe, Ian N
Infiltrating monocytes in liver injury and repair
title Infiltrating monocytes in liver injury and repair
title_full Infiltrating monocytes in liver injury and repair
title_fullStr Infiltrating monocytes in liver injury and repair
title_full_unstemmed Infiltrating monocytes in liver injury and repair
title_short Infiltrating monocytes in liver injury and repair
title_sort infiltrating monocytes in liver injury and repair
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5133365/
https://www.ncbi.nlm.nih.gov/pubmed/27990288
http://dx.doi.org/10.1038/cti.2016.62
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