Molecules involved in the regulation of eosinophil apoptosis.
Apoptosis is the most common form of physiological cell death and a necessary process to maintain cell numbers in multicellular organisms. Eosinophils are constantly produced in the bone marrow and the same numbers die, under normal circumstances, within a relatively short time period. In many eosinophilic inflammatory diseases, reduced eosinophil apoptosis has been described. This mechanism may contribute to increased eosinophil numbers, a phenomenon called eosinophilia. Overexpression of interleukin-5 appears to be crucial for delaying eosinophil apoptosis in many allergic disorders. Survival factor withdrawal leads to the induction of apoptosis. Besides survival cytokines, eosinophil apoptosis is also regulated by death factors. Recent observations suggest a role for mitochondria in conducting eosinophil apoptosis, although the mechanisms that trigger mitochondria to release proapoptotic factors remain less clear. Drugs that specifically induce eosinophil apoptosis might be useful for triggering the resolution of unwanted eosinophilic inflammatory responses.
Simon
Hans-Uwe
HU
Department of Pharmacology, University of Bern, Switzerland. hus@pki.unibe.ch
D017209:Apoptosis; D020169:Caspases / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004804:Eosinophils / Q000166:cytology* / Q000378:metabolism*; D006801:Humans; D008024:Ligands; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism
D016207:Cytokines; D008024:Ligands; D018124:Receptors, Tumor Necrosis Factor; D020169:Caspases