Document Detail


Mechanisms of human eosinophil survival and apoptosis.
MedLine Citation:
PMID:  9179421     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
G M Walsh
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology     Volume:  27     ISSN:  0954-7894     ISO Abbreviation:  Clin. Exp. Allergy     Publication Date:  1997 May 
Date Detail:
Created Date:  1997-07-18     Completed Date:  1997-07-18     Revised Date:  2010-08-25    
Medline Journal Info:
Nlm Unique ID:  8906443     Medline TA:  Clin Exp Allergy     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  482-7     Citation Subset:  IM    
Affiliation:
Department of Respiratory Medicine, University of Leicester, School of Medicine, Glenfield Hospital, UK.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis*
Cell Death
Cell Survival
Eosinophils*
Glucocorticoids / pharmacology
Humans
Signal Transduction
Grant Support
ID/Acronym/Agency:
//Wellcome Trust
Chemical
Reg. No./Substance:
0/Glucocorticoids

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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