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. 2010 Apr;2(2):87-101.
doi: 10.4168/aair.2010.2.2.87. Epub 2010 Mar 24.

Eosinophil survival and apoptosis in health and disease

Affiliations

Eosinophil survival and apoptosis in health and disease

Yong Mean Park et al. Allergy Asthma Immunol Res. 2010 Apr.

Abstract

Eosinophilia is common feature of many disorders, including allergic diseases. There are many factors that influence the production, migration, survival and death of the eosinophil. Apoptosis is the most common form of physiological cell death and a necessary process to maintain but limit cell numbers in humans and other species. It has been directly demonstrated that eosinophil apoptosis is delayed in allergic inflammatory sites, and that this mechanism contributes to the expansion of eosinophil numbers within tissues. Among the proteins known to influence hematopoiesis and survival, expression of the cytokine interleukin-5 appears to be uniquely important and specific for eosinophils. In contrast, eosinophil death can result from withdrawal of survival factors, but also by activation of pro-apoptotic pathways via death factors. Recent observations suggest a role for cell surface death receptors and mitochondria in facilitating eosinophil apoptosis, although the mechanisms that trigger each of these death pathways remain incompletely delineated. Ultimately, the control of eosinophil apoptosis may someday become another therapeutic strategy for treating allergic diseases and other eosinophil-associated disorders.

Keywords: Eosinophils; apoptosis; survival.

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Conflict of interest statement

There are no financial or other issues that might lead to conflict of interest.

Figures

Fig. 1
Fig. 1
From the hematopoietic stem cell to the mature eosinophil.
Fig. 2
Fig. 2
The intracellular signalling pathways of survival-prolonging cytokines IL-3, IL-5 and GM-CSF.
Fig. 3
Fig. 3
Various apoptotic stimuli lead to release of cytochrome.
Fig. 4
Fig. 4
Effects of glucocorticoids in eosinophilic inflammation.

References

    1. Boyce JA, Friend D, Matsumoto R, Austen KF, Owen WF. Differentiation in vitro of hybrid eosinophil/basophil granulocytes: autocrine function of an eosinophil developmental intermediate. J Exp Med. 1995;182:49–57. - PMC - PubMed
    1. Nerlov C, McNagny KM, Doderlein G, Kowenz-Leutz E, Graf T. Distinct C/EBP functions are required for eosinophil lineage commitment and maturation. Genes Dev. 1998;12:2413–2423. - PMC - PubMed
    1. McNagny K, Graf T. Making eosinophils through subtle shifts in transcription factor expression. J Exp Med. 2002;195:F43–F47. - PMC - PubMed
    1. Du J, Stankiewicz MJ, Liu Y, Xi Q, Schmitz JE, Lekstrom-Himes JA, Ackerman SJ. Novel combinatorial interactions of GATA-1, PU.1, and C/EBPepsilon isoforms regulate transcription of the gene encoding eosinophil granule major basic protein. J Biol Chem. 2002;277:43481–43494. - PubMed
    1. Milanovic M, Terszowski G, Struck D, Liesenfeld O, Carstanjen D. IFN consensus sequence binding protein (Icsbp) is critical for eosinophil development. J Immunol. 2008;181:5045–5053. - PubMed