Apoptosis is a physiological method of cell death commonly referred to as 
programmed cell death. However, non-apoptotic programmed cell death, such as 
autophagy and programmed necrosis, has been characterized by morphological 
criteria. In view of the human therapeutic use of DEX, and considering that no 
difference in the number and/or affinity of glucocorticoid receptors in 
activated and non-activated lymphocytes has been reported, we decided to 
evaluate the effect of DEX on fresh peripheral blood mononuclear cells (PBMC). 
Transmission electron microscopy showed that DEX can significantly induce 
apoptosis in non-activated PBMC. It was also observed by transmission electron 
microscopy that, independently of DEX treatment, PBMC also died by a process 
marked by extreme vacuolization and increase in cellular volume; these cells 
were erroneously classified as viable by flow cytometry using the 7-AAD assay. 
It is concluded that the DEX pro-apoptotic effect is not restricted to activated 
PBMC and, therefore, DEX-induced apoptosis could play either homeostatic 
(activated PBMC) or immunosuppressive (non-activated PBMC) roles.