Susceptibility to cytotoxic T lymphocyte-induced apoptosis is a function of the proliferative status of the target

C TLs, which are principal mediators in the elimination of transformed and virus-infected cells from the host, kill their targets by the direct disruption of the plasma membrane and by the induction of the suicide program known as apoptosis (1) (2) (3) (4) . The CTEs arsenal includes the pore-forming protein perforin, a family ofproteases called granzymes, and tumor necrosis factorlike molecules packaged together in cytoplasmic granules (3, 4) . The granule exocytosis model of CTL killing proposes that, upon recognition of viral-or tumor-associated antigen(s) presented via the MHC class I mdecule, the CTL is triggered to release its cytotoxic granule components onto the target cell's plasma membrane. Perforin inserts into the target's plasma membrane and forms transmembrane channds to cause the osmotic lysis of the target (3) . The remaining cytotoxic granule components interact with as yet undefined target cell dements to trigger the apoptotic death of the target, characterized by cellular disintegration and fragmentation of the target's DNA into nudeosome particles (2) (3) (4) .