The cytotoxic CD8(+) T cell population expands considerably during acute im
mune infection with virus. Most of these cells are removed by apoptosis at
the end of the immune response. However, a balance has to be attained betwe
en clearance and retention of a memory population of cells, which respond m
ore rapidly and efficiently to secondary encounter with the antigen. In thi
s article, the role of apoptosis and in particular the development of repli
cative senescence as mechanisms which control this homeostatic balance are
discussed. Although similar mechanisms regulate apoptosis in both humans an
d rodents, the available data suggests that replicative senescence may be c
ontrolled differently in these species, suggesting the there may be differe
nt constraints in the regulation of CD8(+) T cell memory between different
species. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.