T cell apoptosis and reactive oxygen species.

process of activation, division, and differentiation to generate a large pool of activated effector T cells. Regulated induction of apoptosis of these expanded T cells avoids several problems for the host, including increased metabolic cost, disruption of lymphoid homeostasis, and predisposition to autoimmunity and lymphoid neoplasia. On the other hand, it is essential that some activated T cells survive apoptotic death to become memory T cells. Thus, an understanding of why most expanded T cells die, while some survive, will shed light on how autoimmunity and lymphoid cancer are prevented, and how immunity is acquired. Recent studies have identified the molecular details of this apoptotic process that operate in vivo. It is now becoming clear that two separate pathways — activationinduced cell death (AICD) and activated T cell– autonomous death (ACAD) — control the fate of antigen-specific T cells. Interestingly, reactive oxygen species (ROS) can control both pathways through reciprocal modulation of the main effector molecules FasL and Bcl-2. This review will focus on the role played by ROS in the determination of activated T cell fate.