Neutrophil-Derived TNF-Related Apoptosis-Inducing Ligand (TRAIL)

Koga, Yuhki; Matsuzaki, Akinobu; Suminoe, Aiko; Hattori, Hiroyoshi; Hara, Toshiro

doi:10.1158/0008-5472.can-03-1808

Cited by 137 publications

(125 citation statements)

References 36 publications

Supporting

Mentioning

109

Contrasting

Unclassified

Order By: Relevance

“…Consistent with this, blockage of Fas/ FasL function with specific antagonists had no effect on neutrophil spontaneous death [93]. Neutrophils also express other death receptors such as TRAIL-R2 and R3, and their ligand, TNF-related apoptosis-inducing ligand (TRAIL) [98,99]. Neutrophil death can be accelerated by exposure to exogenous TRAIL [98][99][100].…”

Section: Proapoptotic Stimulimentioning

confidence: 88%

“…Neutrophils also express other death receptors such as TRAIL-R2 and R3, and their ligand, TNF-related apoptosis-inducing ligand (TRAIL) [98,99]. Neutrophil death can be accelerated by exposure to exogenous TRAIL [98][99][100]. It has been suggested that TRAIL suppresses certain cytokine-elicited antiapoptotic effects [101,102] and is responsible for neutropenia in systemic lupus erythematosu [103].…”

Section: Proapoptotic Stimulimentioning

confidence: 99%

See 1 more Smart Citation

Constitutive neutrophil apoptosis: Mechanisms and regulation

2007

View full text Add to dashboard Cite

Neutrophil constitutive death is a critical cellular process for modulating neutrophil number and function, and it plays an essential role in neutrophil homeostasis and the resolution of inflammation. Neutrophils die due to programmed cell death or apoptosis. In this article, we review recent studies on the mechanism of neutrophil apoptosis. The involvement of caspase, calpain, reactive oxygen species, cellular survival/death signaling pathways, mitochondria, and BCL-2 family member proteins are discussed. The fate of neutrophils can be influenced within the inflammatory microenvironment. We summarize the current understanding regarding the modulation of neutrophil apoptotic death by various extracellular stimuli such as proinflammatory cytokines, cell adhesion, phagocytosis, red blood cells, and platelets. The involvement of neutrophil apoptosis in infectious and inflammatory diseases is also addressed. Am. J. Hematol. 83:288-295, 2008. V

show abstract

Section: Proapoptotic Stimulimentioning

confidence: 88%

Section: Proapoptotic Stimulimentioning

confidence: 99%

Constitutive neutrophil apoptosis: Mechanisms and regulation

2007

View full text Add to dashboard Cite

show abstract

“…It is noteworthy to point out that molecules other than H 2 O 2 , HOCl and NO· may also mediate the tumoricidal effects of neutrophils. These include proteases [331], membraneperforating agents [331], TNFα [331,332], TRAIL [333] and defensins [334,335].…”

Section: Direct Cytotoxicitymentioning

confidence: 99%

The Multifaceted Roles Neutrophils Play in the Tumor Microenvironment

Sionov

Fridlender

Granot

2014

Cancer Microenvironment

336

261

View full text Add to dashboard Cite

Neutrophils are myeloid cells that constitute 50-70 % of all white blood cells in the human circulation. Traditionally, neutrophils are viewed as the first line of defense against infections and as a major component of the inflammatory process. In addition, accumulating evidence suggest that neutrophils may also play a key role in multiple aspects of cancer biology. The possible involvement of neutrophils in cancer prevention and promotion was already suggested more than half a century ago, however, despite being the major component of the immune system, their contribution has often been overshadowed by other immune components such as lymphocytes and macrophages. Neutrophils seem to have conflicting functions in cancer and can be classified into anti-tumor (N1) and pro-tumor (N2) sub-populations. The aim of this review is to discuss the varying nature of neutrophil function in the cancer microenvironment with a specific emphasis on the mechanisms that regulate neutrophil mobilization, recruitment and activation.

show abstract

“…Furthermore, Koga et al reported that when Jurkat cells, a well-known leukemic cell line susceptible to TRAIL-mediated killing, were cultured with neutrophils in the presence of IFN-γ, the number of Jurkat cells undergoing apoptosis increased [18].…”

Section: Discussionmentioning

confidence: 99%

The release of soluble forms of TRAIL and DR5 by neutrophils of oral cavity cancer patients.

Jabłońska

Jabłoński²,

Marcińczyk³

et al. 2008

Folia Histochem Cytobiol.

View full text Add to dashboard Cite

Abstract:In the present study we examined the release of the soluble form of TRAIL by neutrophils (PMN) derived from patients with oral cavity cancer. Simultaneously, we estimated the ability of PMNs of these patients to release the soluble form of DR5 receptor, a natural regulatory protein of TRAIL. The obtained results were confronted with the serum levels of sTRAIL and sDR5. The cells were isolated from 21 patients with squamous cell carcinoma of oral cavity at diagnosis and three weeks after surgery treatment. For comparative purposes we performed similar examinations in autologous peripheral blood mononuclear cells (PBMC). Cytoplasmic protein fractions of the cells were analyzed for the presence of TRAIL and DR5 by western blotting. Soluble TRAIL and soluble DR5 concentrations in the culture supernatants of cells were confronted with their serum levels using ELISA kit. PMN and PBMC of the whole cancer patient group expressed decreased TRAIL protein and unchanged expression of DR5 receptor in comparison with the control group. Unchanged release of sTRAIL by PMNs of patients in Stage II was accompanying the decrease of the ability of PBMC to secrete this protein. In patients in Stage IV the secretion of sTRAIL by PMNs and PBMC was impaired. In contrast to changes in sTRAIL secretion by PMN and PBMC of oral cavity cancer patients, the secretion of sDR5 by these cells was unchanged. The serum levels of sTRAIL were increased in patients in Stage II before treatment and decreased in the same patients after treatment. The altered ability of PMN of PBMC to secrete sTRAIL may have different implications for the immune response of patients with oral cavity cancer cells at different stages of disease.

show abstract

Neutrophil-Derived TNF-Related Apoptosis-Inducing Ligand (TRAIL)

Cited by 137 publications

References 36 publications

Constitutive neutrophil apoptosis: Mechanisms and regulation

Constitutive neutrophil apoptosis: Mechanisms and regulation

The Multifaceted Roles Neutrophils Play in the Tumor Microenvironment

The release of soluble forms of TRAIL and DR5 by neutrophils of oral cavity cancer patients.

Contact Info

Product

Resources

About