Cell death in allergic diseases |
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Authors: | Hans-Uwe Simon |
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Institution: | (1) Institute of Pharmacology, University of Bern, Friedbühlstrasse 49, CH-3010 Bern, Switzerland |
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Abstract: | 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. |
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Keywords: | Allergy Apoptosis Basophils Caspase Cytokines Dendritic cells Eosinophils Epithelial cells Immune system Inflammation Mast cells Neutrophils Survival factors T cells |
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