Phagocyte recognition of cells undergoing apoptosis

Savill, John; Fadok, Valerie A.; Henson, Peter M.; Haslett, Chris

doi:10.1016/0167-5699(93)90215-7

Cited by 919 publications

(579 citation statements)

References 40 publications

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“…(PS), thrombospondin/CD36 binding site, the vitronectin receptor or CD14, for example (Devitt et al, 1998;Fadok et al, 1992;Savill et al, 1993). Loss of membrane phospholipid asymmetry and consequent exposure of PS in the exoplasmic lea¯et of the plasma membrane is one of the early hallmarks of cells undergoing apoptosis, and is a critical event in their recognition by some macrophage populations (Fadok et al, 1992(Fadok et al, , 1998.…”

Section: Molecular Mechanisms Of Apoptosismentioning

confidence: 99%

Apoptosis in the vasculature: mechanisms and functional importance

Mallat¹,

Tedgui²

2000

British J Pharmacology

304

214

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Apoptotic death has now been recognized in a number of common and threatening vascular diseases, including atherosclerosis. Interest in apoptosis research relates to the fact that apoptosis, in contrast to oncosis, is a highly regulated process of cell death which raises the hope for the development of speci®c therapeutic strategies to alter disease progression. This review summarizes the mechanisms involved in vascular endothelial and smooth muscle cell survival/apoptosis, and the potential roles of apoptotic death in atherosclerosis and restenosis. The potential e ects of modulation of apoptosis in these diseases are also discussed.

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Section: Molecular Mechanisms Of Apoptosismentioning

confidence: 99%

Apoptosis in the vasculature: mechanisms and functional importance

Mallat¹,

Tedgui²

2000

British J Pharmacology

304

214

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“…37 The elimination of apoptotic cells and cell bodies by phagocytes represents an evolutionarily conserved means to prevent exposure of surrounding tissue to potentially cytotoxic, immunogenic or inflammatory cellular content. 38,39 Resolution of inflammation depends not only on the removal of apoptotic cells but also on active suppression of inflammatory mediator production. Aberrations in either mechanism are associated with chronic inflammatory conditions and autoimmune disorders.…”

Section: Introductionmentioning

confidence: 99%

Differential expression in lupus-associated IL-10 promoter single-nucleotide polymorphisms is mediated by poly(ADP-ribose) polymerase-1

et al. 2007

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Systemic lupus erythematosus (SLE) is a complex, multifactorial autoimmune disease characterized by the dysregulation of T and B cells that leads to hyperactivity of B cells and production of autoantibodies, and involves both environmental and genetic factors. Interleukin-10 (IL-10) is a candidate susceptibility gene in SLE. In particular, three IL-10 promoter singlenucleotide polymorphisms (SNPs; À1082A/G, À819T/C and À592A/C) are strongly associated with the pathogenesis of SLE. We found that the homozygous GCC haplotype linked to greater SLE severity confers higher IL-10 gene transcriptional activity than the ATA haplotype in macrophages that encounter apoptotic cells, because of the differential DNA binding to the À592 SNP by a nuclear protein uniquely induced by apoptotic cells. We identified this protein as poly(ADP-ribose) polymerase-1, confirmed its physiological role and characterized its molecular properties in modulating IL-10 production during phagocytosis of apoptotic cells. This study unveils a novel direct link between DNA damage repair/apoptosis pathways and IL-10-mediated immune regulation.

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“…When neutrophils die by apoptosis they retain their granule contents but lose chemotactic and secretory responsiveness [8] and thereafter are recognised and phagocytosed intact by macrophages [9] which fail to release pro-inflammatory mediators in response to this interaction [10]. Although neutrophils un-*Corresponding author.…”

Section: Introductionmentioning

confidence: 99%

Hypoxia prolongs neutrophil survival in vitro

et al. 1995

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~,bstract Neutrophil apoptosis represents a major mechanism ~nvolved in the resolution of inflammation. Since hypoxia induces apoptosis in several cell lines and is of particular relevance in many disease states, we studied the effect of oxygen concentration on neutrophil survival in vitro. Hypoxia caused a dramatic decrease in neutrophil apoptosis (% apoptosis 20 h: 78.7 + 2.2% in 21% 0 2, 61.4 _+ 6.5% in 2.5% 02, 23.1 + 3.2% in 0% 02, = 5). This was additive to the effect of GM-CSF (50 Ulml), not associated with induction of bcl-2 expression, and was not mimicked by methionine (5 raM), superoxide dismutase (200 pg/ml) or Trolox (10 mM) but was mimicked by catalase (250/zg/ml).Hence, hypoxia has a bcl-2-independent effect on neutrophil apoptosis that may adversely affect the clearance of these cells from an inflammatory focus.

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Phagocyte recognition of cells undergoing apoptosis

Cited by 919 publications

References 40 publications

Apoptosis in the vasculature: mechanisms and functional importance

Apoptosis in the vasculature: mechanisms and functional importance

Differential expression in lupus-associated IL-10 promoter single-nucleotide polymorphisms is mediated by poly(ADP-ribose) polymerase-1

Hypoxia prolongs neutrophil survival in vitro

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