Eosinophils play a major role in the onset and maintenance of bronchial inf
lammation and tissue injury in asthma. Like other leukocytes, eosinophils p
resent in excessive numbers in inflamed tissues are removed by apoptosis. T
his phenomenon, also called 'programmed cell death', allows elimination of
dangerous or redundant cells, thereby ensuring maintenance of tissue homeos
tasis. It has been suggested that a defect in eosinophil apoptosis would pa
rticipate in the development and persistence of allergic airways inflammati
on in asthma. Eosinophil apoptosis, as well as the expression and function
of various molecules determining this process, are closely regulated by var
ious stimuli, including cytokines, lipid mediators and growth factors relea
sed by various cell types and by the eosinophil itself, as well as exogenou
s molecules, such as glucocorticoids. These stimuli have been shown to alte
r the expression and function of different molecules involved in the cascad
e of events characterising the apoptotic process, particularly Bcl-2 family
proteins and the pro-apoptotic membrane glycoprotein, Fas. These observati
ons, together with a better understanding of the mechanisms underlying eosi
nophil apoptosis, will help to more clearly define the molecular events inv
olved in accumulation of these cells in blood and tissues and to identify p
otential new targets for the treatment of allergic diseases. (C) 2000 Editi
ons scientifiques et medicales Elsevier SAS.