Veto CTLs induce apoptosis in the effector T cells by a Fas-FasL–mediated mechanism. Upon engagement between the TCR of the effector cell and class I (MHCI) of the veto cell, the effector cell is activated and Fas is up-regulated, allowing for the FasL on the veto CTL to induce apoptosis. However, inhibitors such as FLIP (FADD-like interleukin 1–converting enzyme-inhibitory protein) protect the activated effector T cell. The high affinity afforded by the interaction between CD8 on the veto cell and class I (MHCIα3) on the effector cell enables prolonged association until FLIP is down-regulated and apoptosis can take place. ³⁶