Glutamine protects activated human T cells from apoptosis by up-regulating glutathione and Bcl-2 levels

Glutamine is the most abundant amino acid in the body. A decrease of plasma glutamine concentrations is found in catabolic stress and is related to susceptibility to infections. Glutamine is known to modulate lymphocyte activation; however, little is known about glutamine modulation of cell death of...

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Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 104(2002), 2 vom: 06. Aug., Seite 151-60
1. Verfasser: Chang, Wei-Kuo (VerfasserIn)
Weitere Verfasser: Yang, Kuender D, Chuang, Hau, Jan, Jia-Tsong, Shaio, Men-Fang
Format: Aufsatz
Sprache:English
Veröffentlicht: 2002
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't FASLG protein, human Fas Ligand Protein Interleukin-2 Membrane Glycoproteins Proto-Oncogene Proteins c-bcl-2 fas Receptor Glutamine 0RH81L854J mehr... Ionomycin 56092-81-0 Leukocyte Common Antigens EC 3.1.3.48 Glutathione GAN16C9B8O Tetradecanoylphorbol Acetate NI40JAQ945
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245 1 0 |a Glutamine protects activated human T cells from apoptosis by up-regulating glutathione and Bcl-2 levels 
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520 |a Glutamine is the most abundant amino acid in the body. A decrease of plasma glutamine concentrations is found in catabolic stress and is related to susceptibility to infections. Glutamine is known to modulate lymphocyte activation; however, little is known about glutamine modulation of cell death of activated human T cells. Using Jurkat T cells, we investigated glutamine modulation of T-cell apoptosis activated by PMA plus ionomycin. We found that glutamine at various concentrations significantly enhanced IL-2 production, cell proliferation, and cell viability of Jurkat T cells. Glutamine also decreased the number of apoptotic cells stimulated with PMA plus ionomycin as demonstrated by flow cytometry. Meanwhile, glutamine down-regulated CD95 and CD95L expression, but up-regulated CD45RO and Bcl-2 expression in activated T cells. Further investigation of CD95-mediated caspase activities revealed that supplementation of glutamine significantly decreased caspase-3 and caspase-8 activities in activated T cells. Since oxidative stress is closely associated with induction of lymphocyte apoptosis, we found that glutamine significantly increased glutathione (GSH), but decreased reactive oxygen species levels in activated T cells. Blockade of intracellular GSH formation enhanced, but exogenous GSH supplementation decreased, activated T-cell apoptosis. Studying normal peripheral lymphoproliferation, we also found that the presence of glutamine increased lymphoproliferation as well as Bcl-2 and CD95 expression; but decreased CD95L and activation-induced T-cell death. Taken together, glutamine appeared to augment lymphoproliferation but suppressed activation-induced T-cell death in both Jurkat T cells and human peripheral T lymphocytes 
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700 1 |a Yang, Kuender D  |e verfasserin  |4 aut 
700 1 |a Chuang, Hau  |e verfasserin  |4 aut 
700 1 |a Jan, Jia-Tsong  |e verfasserin  |4 aut 
700 1 |a Shaio, Men-Fang  |e verfasserin  |4 aut 
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