Journal
APOPTOSIS
Volume 9, Issue 5, Pages 515-523Publisher
SPRINGER
DOI: 10.1023/B:APPT.0000038033.14925.02
Keywords
antioxidant; apoptosis; Bcl-2; FasL; reactive oxygen species; ROS; T cell
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Funding
- NIAID NIH HHS [AI 034361] Funding Source: Medline
- NIAMS NIH HHS [AR 47363] Funding Source: Medline
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T cell homeostasis is achieved by balancing the production and proliferation of T cells with their apoptotic cell death. Activation of naive T cells by antigen in the context of MHC results in the massive expansion of antigen-specific T cells and the production of reactive oxygen species (ROS). Following expansion, the majority of the T cells die via apoptosis, while a small number of them survive and differentiate into memory T cells. This cell fate decision is crucial to our understanding of how autoimmunity is avoided and how immunity is maintained. It has become increasingly clear that ROS can affect this cell fate decision by sensitizing T cells to apoptosis. Interestingly, ROS have effects on both intrinsic and extrinsic apoptosis pathways through modulation of expression of the major molecules in these pathways, Bcl-2 and FasL. In this review, we will focus on the pro-apoptotic effects of ROS and mechanisms by which they regulate the death of T cells.
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