Mechanisms of human eosinophil survival and apoptosis.
Eosinophils, with their potentially harmful armoury of toxic products, have available a mechanism by which they can be cleared from the tissues while still intact in the absence of an undesirable pro-inflammatory response. However, our understanding of the induction and control of apoptosis in eosinophils is still incomplete and a great deal of work in this area remains to be done. In other cell types, important regulators of apoptosis have been well characterized. These include the proto-oncogene bcl-2 and related molecules, the family of proteases which share homology with IL-1 beta converting enzyme (ICE) and another protein family which interact with products of the proto-oncogene c-myc. These regulators act at various points on the apoptosis pathway and it appears their interactions are vital in determining whether a cell will survive or die. In particular, the ICE-like proteases have been implicated as a universal apoptosis effector which is associated with the downstream events of programmed cell death [62]. Whether these molecules are involved in the cell death pathway(s) of eosinophils remains to be determined. Much of eosinophilic inflammation might be a result of defects in pathways controlling eosinophil apoptosis and/or their clearance by phagocytes resulting in necrosis and the release of toxic products. A greater understanding of the processes involved in the induction and control of eosinophil apoptosis might provide novel approaches for therapeutic intervention.
Walsh
G M
GM
Department of Respiratory Medicine, University of Leicester, School of Medicine, Glenfield Hospital, UK.
D017209:Apoptosis; D016923:Cell Death; D002470:Cell Survival; D004804:Eosinophils; D005938:Glucocorticoids / Q000494:pharmacology; D006801:Humans; D000090063:Proto-Oncogene Mas; D015398:Signal Transduction
D005938:Glucocorticoids; C000715470:MAS1 protein, human; D000090063:Proto-Oncogene Mas