scholarly journals Activation-induced cell death in murine T cell hybridomas. Differential regulation of Fas (CD95) versus Fas ligand expression by cyclosporin A and FK506

1996 ◽  
Vol 8 (7) ◽  
pp. 1017-1026 ◽  
Author(s):  
Thomas Brunner ◽  
Nam Jin Yoo ◽  
Drake LaFace ◽  
Carl F. Ware ◽  
Douglas R. Green
Keyword(s):  
Cell Death ◽  
T Cell ◽  
Cyclosporin A ◽  
Fas Ligand ◽  
Differential Regulation ◽  
Activation Induced Cell Death ◽  
Ligand Expression

scholarly journals Fas ligand mediates activation-induced cell death in human T lymphocytes.

1995 ◽  
Vol 181 (1) ◽  
pp. 71-77 ◽  
Author(s):  
M R Alderson ◽  
T W Tough ◽  
T Davis-Smith ◽  
S Braddy ◽  
B Falk ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Death ◽  
T Cell ◽  
Fas Ligand ◽  
Significant Proportion ◽  
Cell Receptor ◽  
Target Cells ◽  
Activated T Cells ◽  
Activation Induced Cell Death ◽  
Fas L

A significant proportion of previously activated human T cells undergo apoptosis when triggered through the CD3/T cell receptor complex, a process termed activation-induced cell death (AICD). Ligation of Fas on activated T cells by either Fas antibodies or recombinant human Fas-ligand (Fas-L) also results in cytolysis. We demonstrate that these two pathways of apoptosis are causally related. Stimulation of previously activated T cells resulted in the expression of Fas-L mRNA and lysis of Fas-positive target cells. Fas-L antagonists inhibited AICD of T cell clones and staphylococcus enterotoxin B (SEB)-specific T cell lines. The data indicate AICD in previously stimulated T cells is mediated by Fas/Fas-L interactions.

INTERFERON α AUGMENTS ACTIVATION-INDUCED T CELL DEATH BY UPREGULATION OF FAS (CD95/APO-1) AND FAS LIGAND EXPRESSION

Cytokine ◽  
1999 ◽  
Vol 11 (10) ◽  
pp. 736-743 ◽  
Author(s):  
Arthur Kaser ◽  
Shigekazu Nagata ◽  
Herbert Tilg
Keyword(s):  
Cell Death ◽  
T Cell ◽  
Fas Ligand ◽  
Interferon Α ◽  
Ligand Expression

Cyclosporin A inhibits activation-induced cell death in T-cell hybridomas and thymocytes

Nature ◽  
1989 ◽  
Vol 339 (6226) ◽  
pp. 625-626 ◽  
Author(s):  
Yufang Shi ◽  
Beni M. Sahai ◽  
Douglas R. Green
Keyword(s):  
Cell Death ◽  
T Cell ◽  
Cyclosporin A ◽  
Activation Induced Cell Death

Glucocorticoids inhibit activation-induced cell death (AICD) via direct DNA-dependent repression of the CD95 ligand gene by a glucocorticoid receptor dimer

Blood ◽  
2005 ◽  
Vol 106 (2) ◽  
pp. 617-625 ◽  
Author(s):  
Sven Baumann ◽  
Anja Dostert ◽  
Natalia Novac ◽  
Anton Bauer ◽  
Wolfgang Schmid ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Death ◽  
T Cell ◽  
Glucocorticoid Receptor ◽  
Fas Ligand ◽  
Regulatory Elements ◽  
Activated T Cells ◽  
Activation Induced Cell Death

Abstract Glucocorticoids (GCs) play an important role in the regulation of peripheral T-cell survival. Their molecular mechanism of action and the question of whether they have the ability to inhibit apoptosis in vivo, however, are not fully elucidated. Signal transduction through the glucocorticoid receptor (GR) is complex and involves different pathways. Therefore, we used mice with T-cell-specific inactivation of the GR as well as mice with a function-selective mutation in the GR to determine the signaling mechanism. Evidence is presented for a functional role of direct binding of the GR to 2 negative glucocorticoid regulatory elements (nGREs) in the CD95 (APO-1/Fas) ligand (L) promoter. Binding of GRs to these nGREs reduces activation-induced CD95L expression in T cells. These in vitro results are fully supported by data obtained in vivo. Administration of GCs to mice leads to inhibition of activation-induced cell death (AICD). Thus, GC-mediated inhibition of CD95L expression of activated T cells might contribute to the anti-inflammatory function of steroid drugs. (Blood. 2005;106:617-625)

scholarly journals Regulation of FAS Ligand Expression during Activation-Induced Cell Death in T Cells by p38 Mitogen-Activated Protein Kinase and C-Jun Nh2-Terminal Kinase

2000 ◽  
Vol 191 (6) ◽  
pp. 1017-1030 ◽  
Author(s):  
Jian Zhang ◽  
Jian-Xin Gao ◽  
Kostantin Salojin ◽  
Qing Shao ◽  
Marsha Grattan ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Death ◽  
T Cell ◽  
Protein Kinase ◽  
P38 Mapk ◽  
Fas Ligand ◽  
Mitogen Activated Protein Kinase ◽  
Fasl Expression ◽  
Activation Induced Cell Death ◽  
Mitogen Activated Protein

Activation-induced cell death (AICD) is a mechanism of peripheral T cell tolerance that depends upon an interaction between Fas and Fas ligand (FasL). Although c-Jun NH2-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) may be involved in apoptosis in various cell types, the mode of regulation of FasL expression during AICD in T cells by these two MAPKs is incompletely understood. To investigate the regulatory roles of these two MAPKs, we analyzed the kinetics of TCR-induced p38 MAPK and JNK activity and their regulation of FasL expression and AICD. We report that both JNK and p38 MAPK regulate AICD in T cells. Our data suggest a novel model of T cell AICD in which p38 MAPK acts early to initiate FasL expression and the Fas-mediated activation of caspases. Subsequently, caspases stimulate JNK to further upregulate FasL expression. Thus, p38 MAPK and downstream JNK converge to regulate FasL expression at different times after T cell receptor stimulation to elicit maximum AICD.

T cell receptor-induced Fas ligand expression in cytotoxic T lymphocyte clones is blocked by protein tyrosine kinase inhibitors and cyclosporin A

1994 ◽  
Vol 24 (10) ◽  
pp. 2469-2476 ◽  
Author(s):  
Alberto Anel ◽  
Michel Buferne ◽  
Claude Boyer ◽  
Anne-Marie Schmitt-Verhulst ◽  
Pierre Golstein
Keyword(s):  
T Cell ◽  
Cyclosporin A ◽  
T Cell Receptor ◽  
T Lymphocyte ◽  
Protein Tyrosine Kinase ◽  
Fas Ligand ◽  
Kinase Inhibitors ◽  
Cytotoxic T Lymphocyte ◽  
Cell Receptor ◽  
Ligand Expression

Engagement of the α2β1 integrin inhibits Fas ligand expression and activation-induced cell death in T cells in a focal adhesion kinase-dependent manner

Blood ◽  
2000 ◽  
Vol 95 (6) ◽  
pp. 2044-2051 ◽  
Author(s):  
Fawzi Aoudjit ◽  
Kristiina Vuori
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Cell Death ◽  
T Cell ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Fas Ligand ◽  
Integrin Signaling ◽  
Activation Induced Cell Death ◽  
Fas L

Abstract T-cell receptor (TCR)-mediated apoptosis, also known as activation-induced cell death (AICD), plays an important role in the control of immune response and in the development of T-cell repertoire. Mechanistically, AICD has been largely attributed to the interaction of Fas ligand (Fas-L) with its cell surface receptor Fas in activated T cells. Signal transduction mediated by the integrin family of cell adhesion receptors has been previously shown to modulate apoptosis in a number of different cell types; in T cells, integrin signaling is known to be important in cellular response to antigenic challenge by providing a co-stimulatory signal for TCR. In this study we demonstrate that signaling via the collagen receptor 2β1 integrin specifically inhibits AICD by inhibiting Fas-L expression in activated Jurkat T cells. Engagement of the 2β1 integrin with monoclonal antibodies or with type I collagen, a cognate ligand for 2β1, reduced anti-CD3 and PMA/ionomycin-induced cell death by 30% and 40%, respectively, and the expression of Fas-L mRNA by 50%. Further studies indicated that the 2β1-mediated inhibition of AICD and Fas-L expression required the focal adhesion kinase FAK, a known component in the integrin signaling pathways. These results suggest a role for the 2β1 integrin in the control of homeostasis of immune response and T-cell development.

Engagement of CD44 up-regulates Fas Ligand expression on T cells leading to activation-induced cell death

APOPTOSIS ◽  
2006 ◽  
Vol 12 (1) ◽  
pp. 45-54 ◽  
Author(s):  
Kazuhisa Nakano ◽  
Kazuyoshi Saito ◽  
Shinichiro Mine ◽  
Sho Matsushita ◽  
Yoshiya Tanaka
Keyword(s):  
T Cells ◽  
Cell Death ◽  
Fas Ligand ◽  
Activation Induced Cell Death ◽  
Ligand Expression
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