Cell death in allergic diseases

Simon, Hans-Uwe (2009). Cell death in allergic diseases. Apoptosis, 14(4), pp. 439-46. New York, N.Y.: Springer US; http://www.springer-ny.com 10.1007/s10495-008-0299-1

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Apoptosis, the most common form of cell death, is a key mechanism in the build up and maintenance of both innate and adaptive immunity. Central to the apoptotic process is a family of intracellular cysteine proteases with aspartate-specificity, called caspases. Caspases are counter-regulated by multiple anti-apoptotic molecules, and the expression of the latter in leukocytes is largely dependent on survival factors. Therefore, the physiologic rates of apoptosis change under pathologic conditions. For instance, in inflammation, the expression of survival factors is usually elevated, resulting in increased cell survival and consequently in the accumulation of the involved immune cells. In many allergic diseases, eosinophil apoptosis is delayed contributing to both blood and tissue eosinophilia. Besides eosinophils, apoptosis of other leukocytes is also frequently prevented or delayed during allergic inflammatory processes. In contrast to inflammatory cells, accelerated cell death is often observed in epithelial cells, a mechanism, which amplifies or at least maintains allergic inflammation. In conclusion, deregulated cell death is a common phenomenon of allergic diseases that likely plays an important role in their pathogenesis. Whether the apoptosis is too little or too much depends on the cell type. In this review, we discuss the regulation of the lifespan of the participating leukocytes in allergic inflammatory responses.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Pharmacology

UniBE Contributor:

Simon, Hans-Uwe

ISSN:

1360-8185

Publisher:

Springer US; http://www.springer-ny.com

Language:

English

Submitter:

Factscience Import

Date Deposited:

04 Oct 2013 15:10

Last Modified:

09 Jul 2020 14:52

Publisher DOI:

10.1007/s10495-008-0299-1

PubMed ID:

19130232

Web of Science ID:

000264116600009

BORIS DOI:

10.7892/boris.30718

URI:

https://boris.unibe.ch/id/eprint/30718 (FactScience: 194996)

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