The role of FAS-FAS-ligand(FAS-L) interaction for radiation induced apoptosis in human lymphoma cells

1997 ◽  
Vol 33 ◽  
pp. S22
Author(s):  
C. Belka ◽  
E. Gulbins ◽  
P. Marini ◽  
W. Budach ◽  
F. Lang ◽  
...  
Keyword(s):  
Fas Ligand ◽  
Lymphoma Cells ◽  
Human Lymphoma ◽  
Radiation Induced ◽  
Fas L ◽  
Induced Apoptosis

scholarly journals Peripheral T cells undergoing superantigen-induced apoptosis in vivo express B220 and upregulate Fas and Fas ligand.

1996 ◽  
Vol 183 (2) ◽  
pp. 431-437 ◽  
Author(s):  
T Renno ◽  
M Hahne ◽  
J Tschopp ◽  
H R MacDonald
Keyword(s):  
T Cells ◽  
Fas Ligand ◽  
Apoptotic Cell ◽  
Initial Increase ◽  
Apoptotic Cells ◽  
Peripheral T Cells ◽  
Fas L ◽  
Induced Apoptosis

Staphylococcal enterotoxin B (SEB) is a bacterial superantigen (SAg) that predominantly interacts with V(beta)8+ T cells. In vivo treatment of mice with SEB leads to an initial increase in the percentage of V(beta)8+ T cells, followed by a decrease in the numbers of these cells, eventually reaching lower levels than those found before treatment with the SAg. This decrease is due to apoptosis of the SEB-responding cells. In the present study, we use the distinct light scattering characteristics of apoptotic cells to characterize T cells that are being deleted in response to SEB in vivo. We show that dying, SEB-reactive T cells express high levels of Fas and Fas ligand (Fas-L), which are implicated in apoptotic cell death. In addition, the B cell marker B220 is upregulated on apoptotic cells. Moreover, we show that the generation of cells with an apoptotic phenotype is severely impaired in response to SEB in functional Fas-L-deficient mutant gld mice, confirming the role of the Fas pathway in SAg mediated peripheral deletion in vivo.

Mécanismes de l'apoptose radio-induite

2002 ◽  
Vol 80 (7) ◽  
pp. 629-637 ◽  
Author(s):  
Sarah Baatout ◽  
Hanane Derradji ◽  
Olivier Petitfour ◽  
Hanna von Suchodoletz ◽  
Max Mergeay
Keyword(s):  
Signal Transduction ◽  
Tumor Necrosis ◽  
Fas Ligand ◽  
Signal Transduction Pathways ◽  
Activation Mechanisms ◽  
Radiation Induced ◽  
Clinical Interest ◽  
Induced Apoptosis ◽  
Necrosis Factor

A general overview of the activation mechanisms of programmed cell death or apoptosis following an irradiation is given in this review. First, are summarized the main induction pathways of radiation-induced apoptosis by which extracellular (tumor necrosis factor (TNF), Fas ligand, TNF-related apoptosis-inducing ligand (TRAIL)) and intracellular (mitochondria and caspases) signals are integrated. A second part is then devoted to the importance of p53 and of its regulators (ATR, ATM, DNA-PKcs) in the process of radiation-induced apoptosis. Thereafter, signal transduction pathways and more specially the role of some protein kinases (MEKK, SAPK/JNK, p38-MAPK) is treated. At last, a chapter concerns the clinical interest of radiation-induced apoptosis and the implication of apoptosis in the treatment of certain diseases.Key words: apoptosis, radiation, caspase, p53, mitochondria.

The role of bcl-xL in CD40-mediated rescue from anti-μ-induced apoptosis in WEHI-231 B lymphoma cells

1995 ◽  
Vol 25 (5) ◽  
pp. 1352-1357 ◽  
Author(s):  
Michael S. K. Choi ◽  
Lawrence H. Boise ◽  
Alexander R. Gottschalk ◽  
José Quintans ◽  
Craig B. Thompson ◽  
...  
Keyword(s):  
Lymphoma Cells ◽  
B Lymphoma ◽  
B Lymphoma Cells ◽  
Wehi 231 ◽  
Induced Apoptosis

scholarly journals Induction of Fas (Apo-1, CD95)-Mediated Apoptosis of Activated Lymphocytes by Polyclonal Antithymocyte Globulins

Blood ◽  
1998 ◽  
Vol 91 (7) ◽  
pp. 2360-2368 ◽  
Author(s):  
Laurent Genestier ◽  
Sylvie Fournel ◽  
Monique Flacher ◽  
Olga Assossou ◽  
Jean-Pierre Revillard ◽  
...  
Keyword(s):  
T Cells ◽  
Peripheral Blood ◽  
Fas Ligand ◽  
Mononuclear Cells ◽  
Resting Cells ◽  
Activated T Cells ◽  
Peripheral Blood Mononuclear ◽  
Gene And Protein Expression ◽  
Fas L ◽  
Induced Apoptosis

Polyclonal horse antilymphocyte and rabbit antithymocyte globulins (ATGs) are currently used in severe aplastic anemia and for the treatment of organ allograft acute rejection and graft-versus-host disease. ATG treatment induces a major depletion of peripheral blood lymphocytes, which contributes to its overall immunosuppressive effects. Several mechanisms that may account for lymphocyte lysis were investigated in vitro. At high concentrations (.1 to 1 mg/mL) ATGs activate the human classic complement pathway and induce lysis of both resting and phytohemagglutinin (PHA)-activated peripheral blood mononuclear cells. At low, submitogenic, concentration ATGs induce antibody-dependent cell cytotoxicity of PHA-activated cells, but not resting cells. They also trigger surface Fas (Apo-1, CD95) expression in naive T cells and Fas-ligand gene and protein expression in both naive and primed T cells, resulting in Fas/Fas-L interaction-mediated cell death. ATG-induced apoptosis and Fas-L expression were not observed with an ATG preparation lacking CD2 and CD3 antibodies. Susceptibility to ATG-induced apoptosis was restricted to activated cells, dependent on IL-2, and prevented by Cyclosporin A, FK506, and rapamycin. The data suggest that low doses of ATGs could be clinically evaluated in treatments aiming at the selective deletion of in vivo activated T cells in order to avoid massive lymphocyte depletion and subsequent immunodeficiency.

scholarly journals Differential role of FL-BID and t-BID during verotoxin-1-induced apoptosis in Burkitt’s lymphoma cells

Oncogene ◽  
2018 ◽  
Vol 37 (18) ◽  
pp. 2410-2421 ◽  
Author(s):  
Justine Debernardi ◽  
Emilie Hollville ◽  
Marc Lipinski ◽  
Joëlle Wiels ◽  
Aude Robert
Keyword(s):  
Burkitt’S Lymphoma ◽  
Burkitt's Lymphoma ◽  
Lymphoma Cells ◽  
Induced Apoptosis ◽  
Burkitt’S Lymphoma Cells

The role of the stress-activated protein kinase (SAPK/JNK) signaling pathway in radiation-induced apoptosis

1998 ◽  
Vol 47 (3) ◽  
pp. 225-232 ◽  
Author(s):  
Marcel Verheij ◽  
Gerald A Ruiter ◽  
Shuraila F Zerp ◽  
Wim J van Blitterswijk ◽  
Zvi Fuks ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Signaling Pathway ◽  
Jnk Signaling ◽  
Radiation Induced ◽  
Jnk Signaling Pathway ◽  
Induced Apoptosis

Apoptotic Role of Fas/Fas Ligand System in the Regulation of Erythropoiesis

Blood ◽  
1999 ◽  
Vol 93 (3) ◽  
pp. 796-803 ◽  
Author(s):  
R. De Maria ◽  
U. Testa ◽  
L. Luchetti ◽  
A. Zeuner ◽  
G. Stassi ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Fas Ligand ◽  
Control Mechanism ◽  
Erythroid Differentiation ◽  
Dependent Manner ◽  
Normal Bone ◽  
In Vivo Analysis ◽  
Induced Apoptosis

The possible involvement of Fas and Fas ligand (FasL) in the regulation of erythropoiesis was evaluated. Immunohistochemistry of normal bone marrow specimens revealed that several immature erythroblasts undergo apoptosis in vivo. Analysis of bone marrow erythroblasts and purified progenitors undergoing unilineage erythroid differentiation showed that Fas is rapidly upregulated in early erythroblasts and expressed at high levels through terminal maturation. However, Fas crosslinking was effective only in less mature erythroblasts, particularly at basophilic level, where it induced apoptosis antagonized by high levels of erythropoietin (Epo). In contrast, FasL was selectively induced in late differentiating Fas-insensitive erythroblasts, mostly at the orthochromatic stage. FasL is functional in mature erythroblasts, as it was able to kill Fas-sensitive lymphoblast targets in a Fas-dependent manner. Importantly, FasL-bearing mature erythroblasts displayed a Fas-based cytotoxicity against immature erythroblasts, which was abrogated by high levels of Epo. These findings suggest the existence of a negative regulatory feedback between mature and immature erythroid cells, whereby the former cell population might exert a cytotoxic effect on the latter one in the erythroblastic island. Hypothetically, this negative feedback operates at low Epo levels to moderate the erythropoietic rate; however, it is gradually inhibited at increasing Epo concentrations coupled with enhanced erythrocyte production. Thus, the interaction of Fas and FasL may represent an apoptotic control mechanism for erythropoiesis, contributing to the regulation of red blood cell homeostasis.

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