Maturation of dendritic cells leads to up-regulation of cellular FLICE-inhibitory protein and concomitant down-regulation of death ligand–mediated apoptosis

Leverkus, Martin; Walczak, Henning; McLellan, Alex; Fries, Hans-Werner; Terbeck, Gabi; Bröcker, Eva‐B.; Kämpgen, Eckhart

doi:10.1182/blood.v96.7.2628.h8002628_2628_2631

Cited by 29 publications

(24 citation statements)

References 24 publications

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“…Recent studies have shown that, in addition to its role in limiting growth of cancer cells, TRAIL also has a role in the immune regulation. It induces apoptosis of human peripheral blood lymphocytes and Th1 clones (48,49), of "helpless" CD8 ϩ T cells (50), and immature dendritic cells (51). TRAIL expression has been correlated with allergic inflammation in asthma (52), and TRAIL-R are expressed on eosinophils (24), where they have a prosurvival effect (24,52).…”

Section: Discussionmentioning

confidence: 99%

Human Mast Cells Undergo TRAIL-Induced Apoptosis

Berent-Maoz

Piliponsky

Daigle

et al. 2006

The Journal of Immunology

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Mast cells (MC), supposedly long-lived cells, play a key role in allergy and are important contributors to other inflammatory conditions in which they undergo hyperplasia. In humans, stem cell factor (SCF) is the main regulator of MC growth, differentiation, and survival. Although human MC numbers may also be regulated by apoptotic cell death, there have been no reports concerning the role of the extrinsic apoptotic pathway mediated by death receptors in these cells. We examined expression and function of death receptors for Fas ligand and TRAIL in human MC. Although the MC leukemia cell line HMC-1 and human lung-derived MC expressed both Fas and TRAIL-R, MC lines derived from cord blood (CBMC) expressed only TRAIL-R. Activation of TRAIL-R resulted in caspase 3-dependent apoptosis of CBMC and HMC-1. IgE-dependent activation of CBMC increased their susceptibility to TRAIL-mediated apoptosis. Results suggest that TRAIL-mediated apoptosis may be a mechanism of regulating MC survival in vivo and, potentially, for down-regulating MC hyperplasia in pathologic conditions.

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Section: Discussionmentioning

confidence: 99%

Human Mast Cells Undergo TRAIL-Induced Apoptosis

Berent-Maoz

Piliponsky

Daigle

et al. 2006

The Journal of Immunology

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“…The balance between TRAIL death and decoy receptors was initially considered a possible mechanism whereby cells could negatively regulate TRAIL-induced cytotoxicity, therefore explaining TRAIL selectivity. However, a correlation between this ratio and either protection or susceptibility to apoptosis has never been clearly demonstrated and other mechanisms have been put forward in order to explain the different sensitivity to TRAIL, such as the overexpression of c-FLIP, which could interfere with the activation of caspase-8 [ 23 ].…”

Section: Overview On Trail Biologymentioning

confidence: 99%

TRAIL Modulates the Immune System and Protects against the Development of Diabetes

Bossi

Bernardi

Zauli

et al. 2015

Journal of Immunology Research

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TRAIL or tumor necrosis factor (TNF) related apoptosis-inducing ligand is a member of the TNF superfamily of proteins, whose best characterized function is the induction of apoptosis in tumor, infected, or transformed cells through activation of specific receptors. In nontransformed cells, however, the actions of TRAIL are less well characterized. Recent studies suggest that TRAIL may be implicated in the development and progression of diabetes. Here we review TRAIL biological actions, its effects on the immune system, and how and to what extent it has been shown to protect against diabetes.

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“…Apart from such 'death by neglect', the immune system has several mechanisms for inducing apoptosis. Notably, these include the ligation of certain tumour necrosis factor (TNF) super family receptors, the FAS and TNF receptors; however, ligation of these receptors does not always result in apoptosis; human dendritic cells (DCs) are FAS positive, yet several reports have demonstrated that DCs are resistant to FAS-induced apoptosis [3][4][5]. Indeed, apart from experimentally induced apoptosis or apoptosis caused by factors derived from tumour cells or invading organisms, little is known about endogenous mechanisms for inducing human DC death.…”

Section: Introductionmentioning

confidence: 99%

CD47 Ligation Induces a Rapid Caspase‐Independent Apoptosis‐Like Cell Death in Human Monocytes and Dendritic Cells

2004

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CD47 is a versatile cell-surface molecule expressed on nearly all haematopoietic cells. In its capacity as a thrombospondin-1 (TSP-1) receptor, CD47 has recently been shown to mediate cell death in certain cells, for example, activated but not resting T cells. Here, we have investigated the possibility that human monocytes and dendritic cells (DCs) undergo cell death, following CD47 ligation. Using the TSP-1-derived CD47-binding peptide 4N1K, we found that both freshly isolated monocytes and monocyte-derived DCs underwent a rapid, caspase-independent cell death. This was characterized by the simultaneous presence of phosphatidylserine exposure, plasma membrane permeability, reduced mitochondrial membrane potential and highly fragmented DNA. Not all cells were sensitive to 4N1K-induced apoptosis; a plateau of cell death reached at an average of 38% of the monocyte and DCs populations. The results presented here, thus, show that CD47 can mediate a rapid apoptosislike cell death of human monocytes and DCs.

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Maturation of dendritic cells leads to up-regulation of cellular FLICE-inhibitory protein and concomitant down-regulation of death ligand–mediated apoptosis

Cited by 29 publications

References 24 publications

Human Mast Cells Undergo TRAIL-Induced Apoptosis

Human Mast Cells Undergo TRAIL-Induced Apoptosis

TRAIL Modulates the Immune System and Protects against the Development of Diabetes

CD47 Ligation Induces a Rapid Caspase‐Independent Apoptosis‐Like Cell Death in Human Monocytes and Dendritic Cells

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