scholarly journals Differential ability of T cell subsets to undergo activation-induced cell death

1997 ◽  
Vol 94 (11) ◽  
pp. 5778-5783 ◽  
Author(s):  
A. S. Varadhachary ◽  
S. N. Perdow ◽  
C. Hu ◽  
M. Ramanarayanan ◽  
P. Salgame
Keyword(s):  
Cell Death ◽  
T Cell ◽  
T Cell Subsets ◽  
Activation Induced Cell Death ◽  
Differential Ability

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

Activation-induced cell death in CAR-T cell therapy

Human Cell ◽  
2022 ◽  
Author(s):  
Tian Huan ◽  
Dongfeng Chen ◽  
Guodong Liu ◽  
Hailing Zhang ◽  
Xiaoyan Wang ◽  
...  
Keyword(s):  
Cell Death ◽  
T Cell ◽  
Cell Therapy ◽  
T Cell Therapy ◽  
Car T Cell ◽  
Activation Induced Cell Death ◽  
Car T Cell Therapy ◽  
Car T

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.

CD4+ T-cell help controls CD8+ T-cell memory via TRAIL-mediated activation-induced cell death

Nature ◽  
2005 ◽  
Vol 434 (7029) ◽  
pp. 88-93 ◽  
Author(s):  
Edith M. Janssen ◽  
Nathalie M. Droin ◽  
Edward E. Lemmens ◽  
Michael J. Pinkoski ◽  
Steven J. Bensinger ◽  
...  
Keyword(s):  
Cell Death ◽  
T Cell ◽  
Cd8 T Cell ◽  
Cd4 T Cell ◽  
T Cell Memory ◽  
Cell Memory ◽  
Activation Induced Cell Death ◽  
Cd4 T Cell Help ◽  
Cd8 T Cell Memory ◽  
T Cell Help

scholarly journals High CD3 and ICOS and low TIM-3 expression predict favourable survival in resected oesophageal squamous cell carcinoma

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Min Hee Hong ◽  
Su-Jin Shin ◽  
Sung Kwan Shin ◽  
Dae Joon Kim ◽  
Jae Ill Zo ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Death ◽  
T Cell ◽  
Programmed Cell Death ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Lymphocyte Activation ◽  
Tissue Microarrays ◽  
T Cell Subsets ◽  
Oesophageal Squamous Cell Carcinoma

AbstractWith the increasing oncological potential of immunotherapy, several immune checkpoint modulators are being investigated. The value of immune markers, including programmed cell death ligand-1, programmed cell death-1 (PD-1), inducible co-stimulator (ICOS), lymphocyte activation gene-3, T-cell immunoglobulin, and mucin-dominant containing-3 (TIM-3), is not well known. Using tissue microarrays of 396 patients who underwent surgery for oesophageal squamous cell carcinoma (ESCC), infiltrated T-cell subsets (CD3, CD8, and Foxp3) and checkpoint protein expression were scored. With a median follow-up of 24.8 months, CD3+ TIL subsets (50.0%) had longer median recurrence-free survival (RFS, 55.0 vs 21.4 months) and overall survival (OS, 77.7 vs 35.8 months). Patients with high ICOS expression (46.5%) had longer median RFS (53.9 vs 25.3 months) and OS (88.8 vs 36.9 months). For PD-1, RFS (hazard ratio [HR] 0.67) and OS (HR 0.66) were significantly longer in the high-expression group (45.2%). In the multivariate analysis, high TIM-3 expression (50.8%) had a significant relationship with shorter RFS (HR = 1.52) and OS (HR = 1.60). High CD3+ TIL and T-cell ICOS expression were associated with favourable prognosis, whereas high TIM-3 expression suggested a poor prognosis. Our findings may confer new insights to improve ESCC outcomes beyond the application of PD-1 blockade.

scholarly journals The Caspase 8 Inhibitor c-FLIPL Modulates T-Cell Receptor-Induced Proliferation but Not Activation-Induced Cell Death of Lymphocytes

2002 ◽  
Vol 22 (15) ◽  
pp. 5419-5433 ◽  
Author(s):  
Susanne M. A. Lens ◽  
Takao Kataoka ◽  
Karen A. Fortner ◽  
Antoine Tinel ◽  
Isabel Ferrero ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Death ◽  
T Cell ◽  
T Cell Receptor ◽  
Death Receptor ◽  
Cell Receptor ◽  
Caspase 8 ◽  
Activation Induced Cell Death

ABSTRACT The caspase 8 inhibitor c-FLIPL can act in vitro as a molecular switch between cell death and growth signals transmitted by the death receptor Fas (CD95). To elucidate its function in vivo, transgenic mice were generated that overexpress c-FLIPL in the T-cell compartment (c-FLIPL Tg mice). As anticipated, FasL-induced apoptosis was inhibited in T cells from the c-FLIPL Tg mice. In contrast, activation-induced cell death of T cells in c-FLIPL Tg mice was unaffected, suggesting that this deletion process can proceed in the absence of active caspase 8. Accordingly, c-FLIPL Tg mice differed from Fas-deficient mice by showing no accumulation of B220+ CD4− CD8− T cells. However, stimulation of T lymphocytes with suboptimal doses of anti-CD3 or antigen revealed increased proliferative responses in T cells from c-FLIPL Tg mice. Thus, a major role of c-FLIPL in vivo is the modulation of T-cell proliferation by decreasing the T-cell receptor signaling threshold.

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

p38 MAPK Mediates Inhibition of Activation Induced Cell Death in T Lymphocytes Via Upregulation of Bcl-xL and FLIPshort upon Ligation of CD137/4-1BB or CD28.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3320-3320
Author(s):  
Christian Scholz ◽  
Lilian Stärck ◽  
Mario Lehmann ◽  
Bernd Dörken ◽  
Peter T. Daniel
Keyword(s):  
Cell Death ◽  
T Cell ◽  
Protein Kinase ◽  
T Lymphocytes ◽  
Family Member ◽  
P38 Mapk ◽  
T Cell Activation ◽  
Cell Activation ◽  
Activation Induced Cell Death ◽  
Costimulatory Signals

Abstract Costimulation is essential for the induction of proliferation in naive T cells and for the inhibition of activation induced cell death (AICD) in activated T lymphocytes. While costimulatory signals mediated through the immunglobulin family member CD28 play a prominent role during primary T cell activation, ligation of the tumor necrosis factor receptor family member CD137/4-1BB is more important during late primary and secondary T cell activation. Signals mediated through either costimulatory protein block AICD. Inhibition of AICD through ligation of CD137/4-1BB or CD28 involves upregulation of Bcl-xL and FLIPshort (Eur J Immunol 2005, 35: 1257–66). We further demonstrated that costimulatory signals mediated through CD137/4-1BB or CD28 depend on the activity of phosphatidylinositol 3-kinase and AKT/protein kinase B, two kinases that had formerly been implied in CD28-induced signaling, indicating that CD28- and CD137/4-1BB-mediated signals share downstream signaling pathways. Here, we demonstrate that p38 mitogen-activated protein kinase (MAPK) mediates CD137/4-1BB-induced as well as CD28-mediated costimulation of cell proliferation and inhibition of AICD. This coincides with upregulation of Bcl-xL and FLIPshort. Inhibition of p38 MAPK abrogates T cell receptor induced proliferation and antagonizes costimulation mediated survival. Thus, p38 MAPK, which was previously thought to be primarily involved in CD137/4-1BB-mediated signaling, is similarly important for CD28-induced costimulation and survival. This indicates that, while involving different protein families, signal transduction by CD28 and CD137/4-1BB depends on a common upstream and downstream network of survival kinases.

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