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Front Immunol. 2018 Jan 25;9:44. doi: 10.3389/fimmu.2018.00044. eCollection 2018.

Clearance of Apoptotic Cells by Tissue Epithelia: A Putative Role for Hepatocytes in Liver Efferocytosis.

Author information

1
Centre for Liver Research, College of Medical and Dental Sciences, Institute for Immunology and Immunotherapy, University of Birmingham, Birmingham, United Kingdom.
2
Centre for Liver Research and National Institute for Health Research (NIHR) Birmingham Liver Biomedical Research Unit, College of Medical and Dental Sciences, Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham, United Kingdom.
3
University Hospitals Birmingham NHS Foundation Trust, Birmingham, United Kingdom.

Abstract

Toxic substances and microbial or food-derived antigens continuously challenge the liver, which is tasked with their safe neutralization. This vital organ is also important for the removal of apoptotic immune cells during inflammation and has been previously described as a "graveyard" for dying lymphocytes. The clearance of apoptotic and necrotic cells is known as efferocytosis and is a critical liver function to maintain tissue homeostasis. Much of the research into this form of immunological control has focused on Kupffer cells, the liver-resident macrophages. However, hepatocytes (and other liver resident cells) are competent efferocytes and comprise 80% of the liver mass. Little is known regarding the mechanisms of apoptotic and necrotic cell capture by epithelia, which lack key receptors that mediate phagocytosis in macrophages. Herein, we discuss recent developments that increased our understanding of efferocytosis in tissues, with a special focus on the liver parenchyma. We discuss the impact of efferocytosis in health and in inflammation, highlighting the role of phagocytic epithelia.

KEYWORDS:

apoptosis; cell death; efferocytosis; hepatocytes; liver; necrosis; phagocytosis; regeneration

PMID:
29422896
PMCID:
PMC5790054
DOI:
10.3389/fimmu.2018.00044
[Indexed for MEDLINE]
Free PMC Article

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