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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.
TLDR
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. Expand
C1q and Mannose Binding Lectin Engagement of Cell Surface Calreticulin and Cd91 Initiates Macropinocytosis and Uptake of Apoptotic Cells
TLDR
Evidence is provided that C1q and mannose binding lectin (MBL), a member of the collectin family of proteins, bind to apoptotic cells and stimulate ingestion of these by ligation on the phagocyte surface of the multifunctional protein, calreticulin. Expand
A receptor for phosphatidylserine-specific clearance of apoptotic cells
TLDR
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. Expand
Cell-Surface Calreticulin Initiates Clearance of Viable or Apoptotic Cells through trans-Activation of LRP on the Phagocyte
TLDR
It is demonstrated here that calreticulin acts as a second general recognition ligand by binding and activating LDL-receptor-related protein (LRP) on the engulfing cell, which creates an environment where "don't eat me" signals are rendered inactive and "eat me" signalling signals congregate together and signal for removal. Expand
Exposure of phosphatidylserine on the surface of apoptotic lymphocytes triggers specific recognition and removal by macrophages.
TLDR
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. Expand
Phosphatidylserine-dependent ingestion of apoptotic cells promotes TGF-beta1 secretion and the resolution of inflammation.
TLDR
In vivo that direct instillation of apoptotic cells enhanced the resolution of acute inflammation, and apoptotic cell recognition and clearance, via exposure of PS and ligation of its receptor, induce TGF-beta1 secretion, resulting in accelerated resolution of inflammation. Expand
Macrophage phagocytosis of aging neutrophils in inflammation. Programmed cell death in the neutrophil leads to its recognition by macrophages.
TLDR
Changes in the senescent neutrophil that are associated with their recognition by macrophages are the subject of this investigation, and these processes may represent a mechanism for the removal of neutrophils during inflammation that also serves to limit the degree of tissue injury. Expand
By Binding SIRPα or Calreticulin/CD91, Lung Collectins Act as Dual Function Surveillance Molecules to Suppress or Enhance Inflammation
TLDR
Evidence is provided that SP-A and SP-D act in a dual manner, to enhance or suppress inflammatory mediator production depending on binding orientation, and interaction of these heads with PAMPs on foreign organisms or damaged cells and presentation of the collagenous tails in an aggregated state to calreticulin/CD91, stimulates phagocytosis and proinflammatory responses. Expand
×Phosphorylation of Bax Ser184 by Akt Regulates Its Activity and Apoptosis in Neutrophils*
TLDR
It is suggested that Bax is regulated by phosphorylation of Ser184 in an Akt-dependent manner and thatosphorylation inhibits Bax effects on the mitochondria by maintaining the protein in the cytoplasm, heterodimerized with antiapoptotic Bcl-2 family members. Expand
The Molecular and Cellular Biology of Wound Repair
TLDR
Wound Repair: Overview and General Considerations (R.A.F. Clark), Macrophage Involvement in Wound Repair, Remodeling and Fibrosis, and the Role of Plateletderived Growth Factor in vivo (C.W. Riches). Expand
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