Abstract
Cell death by phagocytosis – termed ‘phagoptosis’ for short – is a form of cell death caused by the cell being phagocytosed i.e. recognised, engulfed and digested by another cell. Phagocytes eat cells that: i) expose ‘eat-me’ signals, ii) lose ‘don’t-eat-me’ signals, and/or iii) bind opsonins. Live cells may express such signals as a result of cell stress, damage, activation or senescence, which can result in phagoptosis. Phagoptosis may be the most abundant form of cell death physiologically as it mediates erythrocyte turnover. It also regulates: reproduction by phagocytosis of sperm, development by removal stem cells and excess cells, and immunity by removal of activated neutrophils and T cells. Phagoptosis mediates the recognition of non-self and host defence against pathogens and cancer cells. However, in inflammatory conditions, excessive phagoptosis may kill our cells, leading to conditions such as hemophagy and neuronal loss.
Keywords: Phagocytosis, apoptosis, cell death, turnover, inflammation, clearance.
Current Molecular Medicine
Title:Phagoptosis - Cell Death By Phagocytosis - Plays Central Roles in Physiology, Host Defense and Pathology
Volume: 15 Issue: 9
Author(s): G. C. Brown, A. Vilalta and M. Fricker
Affiliation:
Keywords: Phagocytosis, apoptosis, cell death, turnover, inflammation, clearance.
Abstract: Cell death by phagocytosis – termed ‘phagoptosis’ for short – is a form of cell death caused by the cell being phagocytosed i.e. recognised, engulfed and digested by another cell. Phagocytes eat cells that: i) expose ‘eat-me’ signals, ii) lose ‘don’t-eat-me’ signals, and/or iii) bind opsonins. Live cells may express such signals as a result of cell stress, damage, activation or senescence, which can result in phagoptosis. Phagoptosis may be the most abundant form of cell death physiologically as it mediates erythrocyte turnover. It also regulates: reproduction by phagocytosis of sperm, development by removal stem cells and excess cells, and immunity by removal of activated neutrophils and T cells. Phagoptosis mediates the recognition of non-self and host defence against pathogens and cancer cells. However, in inflammatory conditions, excessive phagoptosis may kill our cells, leading to conditions such as hemophagy and neuronal loss.
Export Options
About this article
Cite this article as:
Brown G. C., Vilalta A. and Fricker M., Phagoptosis - Cell Death By Phagocytosis - Plays Central Roles in Physiology, Host Defense and Pathology, Current Molecular Medicine 2015; 15 (9) . https://dx.doi.org/10.2174/156652401509151105130628
DOI https://dx.doi.org/10.2174/156652401509151105130628 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
HGF-Antagonists: Structure, Activities, and Anti-cancer Approach
Current Signal Transduction Therapy Preparation and Biodistribution of Technetium-99m-Labeled Bis- Misonidazole (MISO) as an Imaging Agent for Tumour Hypoxia
Medicinal Chemistry Identification of Functional Peptides from Natural and Synthetic Products on Their Anticancer Activities by Tumor Targeting
Current Medicinal Chemistry Resveratrol in Cancer: Cellular and Mitochondrial Consequences of Proton Transport Inhibition
Current Pharmaceutical Design Epigenetics in Clinical Management of Children and Adolescents with Brain Tumors
Current Cancer Drug Targets Antibody Engineering, Virus Retargeting and Cellular Immunotherapy: One Ring to Rule Them All?
Current Gene Therapy The Need for Calcium Channels in Cell Proliferation
Recent Patents on Anti-Cancer Drug Discovery Blockage of Autophagy in C6 Glioma Cells Enhanced Radiosensitivity Possibly by Attenuating DNA-PK-Dependent DSB Due to Limited Ku Nuclear Translocation and DNA Binding
Current Molecular Medicine Voltage-Dependent Potassium Channels Kv1.3 and Kv1.5 in Human Cancer
Current Cancer Drug Targets Natural Product-Derived Small Molecule Activators of Hypoxia-Inducible Factor-1 (HIF-1)
Current Pharmaceutical Design MtDNA As a Cancer Marker: A Finally Closed Chapter?
Current Genomics Pharmacogenomics of Non-Small Cell Lung Cancer
Current Pharmacogenomics Tumor-Targeting Peptides: Ligands for Molecular Imaging and Therapy
Anti-Cancer Agents in Medicinal Chemistry Longitudinal Melatonin Production in Female Laboratory Rats During 1997-2006: Possible Modulatory Effects of Changing Solar Activity
Current Aging Science Dendrimers as Novel Systems for Delivery of Neuropharmaceuticals to the Brain
CNS & Neurological Disorders - Drug Targets Recent Advances in Targeting Nuclear Molecular Imaging Driven by Tetrazine Bioorthogonal Chemistry
Current Medicinal Chemistry Mucoadhesive Chitosan Derivatives as Novel Drug Carriers
Current Pharmaceutical Design microRNAs, Gap Junctional Intercellular Communication and Mesenchymal Stem Cells in Breast Cancer Metastasis
Current Cancer Therapy Reviews Anticancer Peptides and Proteins: A Panoramic View
Protein & Peptide Letters Osteoinductive Small Molecules: Growth Factor Alternatives for Bone Tissue Engineering
Current Pharmaceutical Design