Deletion of self-reactive clones of immature thymocytes by activation-
induced death (AID) is thought to be the primary mechanism for the est
ablishment of self-tolerance in the T-cell compartment. Recent evidenc
e suggests that a genetically distinct but analogous process of AID in
mature T cells is important in regulating peripheral immune responses
. AID of peripheral T cells requires the expression of functional Fas
and Fas ligand by the T-cell population. As qualitatively similar sign
als from the TCR are responsible for both T-cell expansion in inflamma
tion and T-cell elimination by AID, regulating the balance between the
se opposing functions plays a crucial role in successful responses to
pathogens and tumors while minimizing autoimmunity.