Immunological Tolerance by Antigen-Induced Apoptosis of Mature T Lymphocytes

1994 ◽  
pp. 81-89 ◽  
Author(s):  
Lixin Zheng ◽  
Stefen A. Boehme ◽  
Jeffrey M. Critchfield ◽  
Juan Carlos Zuniga-Pflucker ◽  
Matthew Freedman ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Immunological Tolerance ◽  
Induced Apoptosis

scholarly journals Macrophage-dependent Apoptosis of CD4+ T Lymphocytes from HIV-infected Individuals Is Mediated by FasL and Tumor Necrosis Factor

1997 ◽  
Vol 185 (1) ◽  
pp. 55-64 ◽  
Author(s):  
Andrew D. Badley ◽  
David Dockrell ◽  
Margaret Simpson ◽  
Ron Schut ◽  
David H. Lynch ◽  
...  
Keyword(s):  
T Cells ◽  
Tumor Necrosis Factor ◽  
T Lymphocytes ◽  
Cd4 T Cells ◽  
Tumor Necrosis ◽  
Human Macrophages ◽  
Infected Cells ◽  
Induced Apoptosis ◽  
Antigen Presenting ◽  
Necrosis Factor

Apoptosis of bystander uninfected CD4+ T lymphocytes by neighboring HIV-infected cells is observed in cell culture and in lymphoid tissue of HIV-infected individuals. This study addresses whether antigen-presenting cells such as human macrophages mediate apoptosis of CD4+ T cells from HIV-infected individuals. Uninfected human macrophages, and to a larger degree, HIV-infected macrophages mediate apoptosis of T cells from HIV-infected, but not from uninfected control individuals. This macrophage-dependent killing targets CD4+, but not CD8+ T lymphocytes from HIV-infected individuals, and direct contact between macrophages and lymphocytes is required. Additional analyses indicated that the apoptosis-inducing ligands, FasL and tumor necrosis factor (TNF), mediate this macrophage-induced apoptosis of CD4+ T cells. These results support a role for macrophage-associated FasL and TNF in the selective depletion of CD4+ T cells in HIV-infected individuals.

scholarly journals Primary Human T Lymphocytes Engineered with a Codon-Optimized IL-15 Gene Resist Cytokine Withdrawal-Induced Apoptosis and Persist Long-Term in the Absence of Exogenous Cytokine

2005 ◽  
Vol 175 (11) ◽  
pp. 7226-7234 ◽  
Author(s):  
Cary Hsu ◽  
Marybeth S. Hughes ◽  
Zhili Zheng ◽  
Regina B. Bray ◽  
Steven A. Rosenberg ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Human T Lymphocytes ◽  
Exogenous Cytokine ◽  
Induced Apoptosis

Endotoxemia-induced Lymphocyte Apoptosis Is Augmented by a Hyperinsulinemic–Euglycemic Clamp

2005 ◽  
Vol 102 (4) ◽  
pp. 768-773 ◽  
Author(s):  
Jeppe Sylvest Nielsen ◽  
Anders Larsson ◽  
Vibeke Brix-Christensen ◽  
Jens Randel Nyengaard ◽  
Thomas Ledet ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Confidence Interval ◽  
Intervention Group ◽  
Lymphocyte Apoptosis ◽  
Euglycemic Clamp ◽  
Group 4 ◽  
Hyperinsulinemic Euglycemic Clamp ◽  
Group 2 ◽  
Induced Apoptosis ◽  
B And T Lymphocytes

Background Sepsis and endotoxemia are associated with lymphocyte apoptosis. This has been regarded as harmful, contributing to further immune suppression in already immune-compromised patients. Because normalization of blood glucose improves outcome in critically ill patients, the authors hypothesized that one of the effects of insulin and normoglycemia would be inhibition of lymphocyte apoptosis. Therefore, in this experimental study in pigs, the authors examined the separate and combined effects of acute endotoxemia and a hyperinsulinemic-euglycemic clamp (HEC) on lymphocyte apoptosis. Methods After 60 min of stabilization, 38 anesthetized and mechanically ventilated pigs (weight, 35-40 kg) were divided (by randomization performed before the experiment) into four groups and were then studied for 570 min. Group 1 received no intervention. Group 2 received a HEC (5 mm p-glucose, insulin infusion rate of 0.6 mU . kg (-1). min(-1)) for 570 min. Group 3 received a lipopolysaccharide infusion for 180 min. Group 4 was given a combination of a HEC and a lipopolysaccharide infusion. After the 570-min study period, the pigs were killed, and tissue was sampled from the spleen and frozen. In four sections of each sample, the apoptosis of B and T lymphocytes were analyzed using stereologic methods: The number of apoptotic B and T cells was estimated by fluorescence immunohistochemistry with anti-active caspase-3 and either anti-CD21 (B lymphocytes) or anti-CD3epsilon (T lymphocytes). The number of apoptotic B and T lymphocytes was then compared using two-way analysis of variance, and the interaction between endotoxemia and the clamp (hyperinsulinemia and euglycemia) was investigated. Results Endotoxemia induced apoptosis of B (P < 0.001) and T lymphocytes (P = 0.016) in the spleen, and this effect was independent of the clamp. The ratios of apoptotic cells in the spleen tissue of pigs with and without endotoxemia were 2.4 (confidence interval, 1.7-3.4) and 1.6 (confidence interval, 1.1-2.2) for B and T lymphocytes, respectively. Independent of endotoxin infusion, HEC increased the number of apoptotic lymphocytes (P = 0.029 and P = 0.038 for B and T lymphocytes, respectively). The ratios of the number of apoptotic spleen cells in pigs treated and not treated with HEC were 1.5 (confidence interval, 1.0-2.1) and 1.5 (confidence interval, 1.0-2.1) for B and T lymphocytes, respectively. Conclusion In this porcine model, both endotoxemia and a HEC increased the number of apoptotic B and T lymphocytes in the spleen. Contrary to our hypothesis, lymphocyte apoptosis during acute endotoxemia was augmented by a HEC.

Cardiotoxin-III selectively enhances activation-induced apoptosis of human CD8+ T lymphocytes

2003 ◽  
Vol 193 (1) ◽  
pp. 97-105 ◽  
Author(s):  
Shu-Hui Su ◽  
Shu-Jem Su ◽  
Shinne-Ren Lin ◽  
Kee-Lung Chang
Keyword(s):  
T Lymphocytes ◽  
Cd8 T Lymphocytes ◽  
Induced Apoptosis

Volatile Anesthetics Induce Caspase-dependent, Mitochondria-mediated Apoptosis in Human T Lymphocytes In Vitro 

2005 ◽  
Vol 102 (6) ◽  
pp. 1147-1157 ◽  
Author(s):  
Torsten Loop ◽  
David Dovi-Akue ◽  
Michael Frick ◽  
Martin Roesslein ◽  
Lotti Egger ◽  
...  
Keyword(s):  
Membrane Potential ◽  
T Lymphocytes ◽  
Cytochrome C ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
Volatile Anesthetics ◽  
Human T Lymphocytes ◽  
Induced Apoptosis

Background Volatile anesthetics modulate lymphocyte function during surgery, and this compromises postoperative immune competence. The current work was undertaken to examine whether volatile anesthetics induce apoptosis in human T lymphocytes and what apoptotic signaling pathway might be used. Methods Effects of sevoflurane, isoflurane, and desflurane were studied in primary human CD3 T lymphocytes and Jurkat T cells in vitro. Apoptosis and mitochondrial membrane potential were assessed using flow cytometry after green fluorescent protein-annexin V and DiOC6-fluorochrome staining. Activity and proteolytic processing of caspase 3 was measured by cleaving of the fluorogenic effector caspase substrate Ac-DEVD-AMC and by anti-caspase-3 Western blotting. Release of mitochondrial cytochrome c was studied after cell fractionation using anti-cytochrome c Western blotting and enzyme-linked immunosorbent assays. Results Sevoflurane and isoflurane induced apoptosis in human T lymphocytes in a dose-dependent manner. By contrast, desflurane did not exert any proapoptotic effects. The apoptotic signaling pathway used by sevoflurane involved disruption of the mitochondrial membrane potential and release of cytochrome c from mitochondria to the cytosol. In addition, the authors observed a proteolytic cleavage of the inactive p32 procaspase 3 to the active p17 fragment, increased caspase-3-like activity, and cleavage of the caspase-3 substrate poly-ADP-ribose-polymerase. Sevoflurane-induced apoptosis was blocked by the general caspase inhibitor Z-VAD.fmk. Death signaling was not mediated via the Fas/CD95 receptor pathway because neither anti-Fas/CD95 receptor antagonism nor FADD deficiency or caspase-8 deficiency were able to attenuate sevoflurane-mediated apoptosis. Conclusion Sevoflurane and isoflurane induce apoptosis in T lymphocytes via increased mitochondrial membrane permeability and caspase-3 activation, but independently of death receptor signaling.

Artificial mitochondria transfer prevents staurosporine-induced apoptosis of human T lymphocytes.

Cytotherapy ◽  
2019 ◽  
Vol 21 (5) ◽  
pp. e8
Author(s):  
E. Parra ◽  
A. LeGatt ◽  
A. Court ◽  
F.E. Figueroa ◽  
M. Khoury
Keyword(s):  
T Lymphocytes ◽  
Human T Lymphocytes ◽  
Mitochondria Transfer ◽  
Induced Apoptosis

GILZ, a new target for the transcription factor FoxO3, protects T lymphocytes from interleukin-2 withdrawal–induced apoptosis

Blood ◽  
2004 ◽  
Vol 104 (1) ◽  
pp. 215-223 ◽  
Author(s):  
Marie-Liesse Asselin-Labat ◽  
Muriel David ◽  
Armelle Biola-Vidamment ◽  
Damiana Lecoeuche ◽  
Maria-Christina Zennaro ◽  
...  
Keyword(s):  
Cell Death ◽  
T Lymphocytes ◽  
Leucine Zipper ◽  
Interleukin 2 ◽  
Cell Receptor ◽  
Receptor Activation ◽  
Forkhead Box ◽  
Activated T Lymphocytes ◽  
Functional Consequences ◽  
Induced Apoptosis

Abstract Interleukin-2 (IL-2) withdrawal is a physiologic process inducing cell death in activated T lymphocytes. Glucocorticoid-induced leucine zipper (GILZ) has recently been identified as a protein modulating T-cell receptor activation by repressing various signaling pathways. We report here that IL-2 deprivation leads to expression of GILZ in T lymphocytes. We then characterized the human gilz promoter and showed that FoxO3 (Forkhead box class O3) binding to the Forkhead responsive elements identified in the promoter is necessary for induction of gilz expression upon IL-2 withdrawal. To assess the functional consequences of this induction, we used 2 strategies, GILZ overexpression and GILZ silencing in murine IL-2–dependent CTLL-2 cells. GILZ overexpression protects CTLL-2 cells from IL-2 withdrawal–induced apoptosis, whereas cell death is accelerated in cells unable to express GILZ. Concomitantly, the expression of Bim is inhibited in GILZ-overexpressing cells and enhanced when GILZ expression is impaired. Furthermore, GILZ inhibits FoxO3 transcriptional activity that leads to inhibition of Bim expression but also to down-regulation of GILZ itself. Therefore, GILZ is a transiently expressed protein induced upon IL-2 withdrawal that protects T cells from the onset of apoptosis.

An IRF-1-dependent pathway of DNA damage-induced apoptosis in mitogen-activated T lymphocytes

Nature ◽  
1995 ◽  
Vol 376 (6541) ◽  
pp. 596-599 ◽  
Author(s):  
Tomohiko Tamura ◽  
Masahiko Ishihara ◽  
Marc S. Lamphier ◽  
Nobuyuki Tanaka ◽  
Isao Oishi ◽  
...  
Keyword(s):  
Dna Damage ◽  
T Lymphocytes ◽  
Activated T Lymphocytes ◽  
Induced Apoptosis ◽  
Dependent Pathway

Effect of oesophagectomy on monocyte-induced apoptosis of peripheral blood T lymphocytes

2001 ◽  
Vol 88 (8) ◽  
pp. 1110-1116 ◽  
Author(s):  
K. Kono ◽  
A. Takahashi ◽  
H. Iizuka ◽  
H. Fujii ◽  
T. Sekikawa ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Peripheral Blood ◽  
Induced Apoptosis

7,8-dihydroneopterin-induced apoptosis in Jurkat T lymphocytes: a comparison with anti-Fas- and hydrogen peroxide-mediated cell death

1998 ◽  
Vol 56 (9) ◽  
pp. 1181-1187 ◽  
Author(s):  
Barbara Wirleitner ◽  
Gabriele Baier-Bitterlich ◽  
Günther Böck ◽  
Bernhard Widner ◽  
Dietmar Fuchs
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Death ◽  
T Lymphocytes ◽  
Induced Apoptosis
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