Abstract
The regulated initiation of programs leading to cell death is responsible, at least in part, for maintaining homeostasis within the immune system. Two general mechanisms for the production of cytotoxicity in susceptible targets by T effector cells have been described, one involving Ca++ dependent, perforin/granzyme exocytosis, and the other involving Fas antigen (CD95) engagement1. Fas functions in target cells as a receptor that signals for apoptosis, and Fas has been implicated in the process of reducing lymphocyte numbers following acute immune responses, termed activation induced cell death2–8. Although classical CD8+ cytotoxic T lymphocytes have recently been shown to express both types of cytotoxic activity, a distinct class of T cells, with the phenotype of CD4+ Th1 cells, mediates target cell death primarily in a Fas-dependent fashion.