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Reactive oxygen species regulate activation-induced T cell apoptosis
D A Hildeman1, T Mitchell, T K Teague
1Howard Hughes Medical Institute, Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado 80206, USA.
Immunity
|July 14, 1999
Summary
Reactive oxygen species (ROS) cause activated T cell death through mitochondrial damage and DNA fragmentation. A superoxide dismutase mimetic (MnTBAP) protected these cells, indicating ROS role in T cell apoptosis.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Reactive oxygen species (ROS) are known to induce apoptosis in various cell types.
- Understanding the role of ROS in T cell apoptosis is crucial for immune regulation.
Purpose of the Study:
- To investigate the specific role of ROS in the apoptosis of activated T cells.
- To elucidate the mechanisms by which ROS contribute to T cell death.
Main Methods:
- T cells were activated in vivo and then cultured ex vivo.
- Assessed cell death markers including mitochondrial transmembrane potential (Δψm) loss, caspase-dependent DNA fragmentation, and superoxide generation.
- Utilized a superoxide dismutase mimetic, MnTBAP, to evaluate the protective effects against ROS-induced apoptosis.
Main Results:
- Activated T cells underwent apoptosis independently of Fas and TNF-alpha signaling pathways.
- Apoptosis was characterized by rapid loss of Δψm, caspase-dependent DNA fragmentation, and significant superoxide generation.
- Treatment with MnTBAP effectively prevented superoxide generation, DNA loss, Δψm reduction, and subsequent cell death.
Conclusions:
- ROS play a significant role in regulating caspase activation and apoptosis in activated T cells.
- Superoxide generation by ROS contributes to peripheral T cell deletion, highlighting a potential mechanism for immune homeostasis.