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
-
Possible Targets of Herbals for Type 3 Diabetes: A Review
Current Traditional Medicine CCL21 and IFNγ Recruit and Activate Tumor Specific T cells in 3D Scaffold Model of Breast Cancer
Anti-Cancer Agents in Medicinal Chemistry Inhibiting the “Undruggable” RAS/Farnesyltransferase (FTase) Cancer Target by Manumycin-related Natural Products
Current Medicinal Chemistry Nutlins and Ionizing Radiation in Cancer Therapy
Current Pharmaceutical Design Protein Kinase C as a Drug Target Implications for Drug or Diet Prevention and Treatment of Cancer
Current Drug Targets 3D-QSAR and Docking Studies of 4-morpholinopyrrolopyrimidine Derivatives as Potent mTOR Inhibitors
Letters in Drug Design & Discovery Turning Tumor-Promoting Copper into an Anti-Cancer Weapon via High-Throughput Chemistry
Current Medicinal Chemistry Lectin Techniques for Glycoproteomics
Current Proteomics Autophagy Regulators as Potential Cancer Therapeutic agents: A Review
Current Topics in Medicinal Chemistry Drug Delivery Nanoparticles in Treating Chemoresistant Tumor Cells
Current Medicinal Chemistry The Delivery of Biologically Active (Therapeutic) Peptides and Proteins into Cells
Current Medicinal Chemistry Dependence of DPPH Radical Scavenging Activity of Dietary Flavonoid Quercetin on Reaction Environment
Mini-Reviews in Medicinal Chemistry Recent Advances on Small-Molecule Survivin Inhibitors
Current Medicinal Chemistry ER Stress and Autophagy
Current Molecular Medicine Metastatic Cancer Stem Cells: New Molecular Targets for Cancer Therapy
Current Pharmaceutical Biotechnology Human Cytomegalovirus US28: A Functionally Selective Chemokine Binding Receptor
Infectious Disorders - Drug Targets Lipid-based siRNA Delivery Systems: Challenges, Promises and Solutions Along the Long Journey
Current Pharmaceutical Biotechnology Experimental Therapy for Lung Cancer: Umbilical Cord-Derived Mesenchymal Stem Cell-Mediated Interleukin-24 Delivery
Current Cancer Drug Targets The Hippocampal Autophagic Machinery is Depressed in the Absence of the Circadian Clock Protein PER1 that may Lead to Vulnerability During Cerebral Ischemia
Current Neurovascular Research Amino Acid Transporter-Targeted Radiotracers for Molecular Imaging in Oncology
Current Medicinal Chemistry