Abstract Monocyte apoptosis has emerged as a central regulatory event in hemopoiesis and inflammation.
Inflammatory cytokines can either promote or prevent monocyte apoptosis.
Engagement of the Fas Ag resulted in apoptosis of monocytes, as monitored by propidium iodide uptake, decrease in cell size, DNA fragmentation, and characteristic ultrastructural changes. Moreover, the exogenous addition of hydrogen peroxide or menadione, an intracellular generator of superoxide anion, was sufficient for the induction of monocyte apoptosis. These data indicate that ROI are key mediators of Fas-induced apoptosis. Therefore, monocytes appear to have a protective mechanism that can interfere directly with the Fas-induced pathway of cell suicide, thereby controlling their destiny.