| Mechanisms of human eosinophil survival and apoptosis. | |
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MedLine Citation:
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PMID: 9179421 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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G M Walsh |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Review |
Journal Detail:
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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:
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Created Date: 1997-07-18 Completed Date: 1997-07-18 Revised Date: 2010-08-25 |
Medline Journal Info:
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Nlm Unique ID: 8906443 Medline TA: Clin Exp Allergy Country: ENGLAND |
Other Details:
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Languages: eng Pagination: 482-7 Citation Subset: IM |
Affiliation:
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Department of Respiratory Medicine, University of Leicester, School of Medicine, Glenfield Hospital, UK. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Apoptosis* Cell Death Cell Survival Eosinophils* Glucocorticoids / pharmacology Humans Signal Transduction |
| Grant Support | |
ID/Acronym/Agency:
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//Wellcome Trust |
| Chemical | |
Reg. No./Substance:
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0/Glucocorticoids |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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