It has recently been recognized that extravasated granulocytes undergo
apoptosis or programmed cell death. This process controls the functio
nal longevity of these cells and is exquisitely modulated by environme
ntal inflammatory mediators. By contrast with nemesis, an alternative
fate for granulocytes in tissues, during apoptosis the granulocyte mem
brane remains intact and potentially injurious granule contents are re
tained. The intact apoptotic cell is removed by macrophages utilizing
novel surface recognition mechanisms which fail to trigger a pro-infla
mmatory macrophage response. The balance between granulocyte apoptosis
and necrosis in inflamed tissues may be an important determinant of t
he degree of tissue injury, and further dissection of the mechanisms o
f granulocyte apoptosis and removal may lead to new therapeutic strate
gies in inflammatory disease.