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Open AccessJournal ArticleDOI

Clearance of Apoptotic Cells: Getting Rid of the Corpses

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TLDR
In this article, the authors present a simplified model of the phagocytic synapse and discuss the role of lysophosphatidylcholine as soluble attraction signal in the removal of apoptotic cells.
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This article is published in Molecular Cell.The article was published on 2004-05-07 and is currently open access. It has received 568 citations till now. The article focuses on the topics: Apoptotic cell clearance & Tissue homeostasis.

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Resolution of inflammation: the beginning programs the end.

TL;DR: Emerging evidence now suggests that an active, coordinated program of resolution initiates in the first few hours after an inflammatory response begins, and the mechanism required for inflammation resolution may underpin the development of drugs that can resolve inflammatory processes in directed and controlled ways.
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Nucleotides released by apoptotic cells act as a find-me signal to promote phagocytic clearance

TL;DR: Nucleotides are identified as a critical find-me cue released by apoptotic cells to promote P2Y2-dependent recruitment of phagocytes, and provide evidence for a clear relationship between a find- me signal and efficient corpse clearance in vivo.
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Overview of cell death signaling pathways

TL;DR: Changing attention is being focused on alternative signaling pathways leading to cell death including necrosis, autophagy, and mitotic catastrophe.
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Journal Article

Exposure of phosphatidylserine on the surface of apoptotic lymphocytes triggers specific recognition and removal by macrophages.

TL;DR: The data suggest that macrophages specifically recognize phosphatidylserine that is exposed on the surface of lymphocytes during the development of apoptosis, and suggest that apoptotic lymphocytes lose membrane phospholipid asymmetry and expose phosphorus on the outer leaflet of the plasma membrane.
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Macrophages that have ingested apoptotic cells in vitro inhibit proinflammatory cytokine production through autocrine/paracrine mechanisms involving TGF-beta, PGE2, and PAF.

TL;DR: The results suggest that binding and/or phagocytosis of apoptotic cells induces active antiinflammatory or suppressive properties in human macrophages, likely that resolution of inflammation depends not only on the removal of apoptosis but on active suppression of inflammatory mediator production.
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Immunosuppressive effects of apoptotic cells

TL;DR: The presence of apoptotic cells during monocyte activation increases their secretion of the anti-inflammatory and immunoregulatory cytokine interleukin 10 (IL-10) and decreases secretion ofthe proinflammatory cytokines tumour necrosis factor-α (TNF-α), IL-1 and IL-12, which may inhibit inflammation and contribute to impaired cell-mediated immunity in conditions associated with increased apoptosis.
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Autoantigens targeted in systemic lupus erythematosus are clustered in two populations of surface structures on apoptotic keratinocytes.

TL;DR: Systemic lupus erythematosus is a multisystem autoimmune disease in which the autoantibody response targets a variety of autoantigens of diverse subcellular location, and it is shown that they are clustered in two distinct populations of blebs at the surface of apoptotic cells.
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A receptor for phosphatidylserine-specific clearance of apoptotic cells

TL;DR: Using phage display, a gene that appears to recognize phosphatidylserine on apoptotic cells is cloned and shown to be highly homologous to genes of unknown function in Caenorhabditis elegans and Drosophila melanogaster, suggesting that phosphatido-serine recognition on apoptosis cells during their removal by phagocytes is highly conserved throughout phylogeny.
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