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Critical Reviews™ in Immunology
Fator do impacto: 1.404 FI de cinco anos: 3.347 SJR: 0.706 SNIP: 0.55 CiteScore™: 2.19

ISSN Imprimir: 1040-8401
ISSN On-line: 2162-6472

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Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.2017020172
pages 429-444

Essential Mechanisms of Differential Activation of Eosinophils by IL-3 Compared to GM-CSF and IL-5

Stephane Esnault
University of Wisconsin-Madison School of Medicine and Public Health, Department of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, 600 Highland Avenue, CSC K4/928, Madison, WI 53792-9988
Elizabeth A. Kelly
University of Wisconsin-Madison School of Medicine and Public Health, Department of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, 600 Highland Avenue, CSC K4/928, Madison, WI 53792-9988

RESUMO

Compelling evidence has demonstrated that the eosinophils bring negative biological outcomes in several diseases, including eosinophilic asthma and hypereosinophilic syndromes. Eosinophils produce and store a broad range of toxic proteins and other mediators that enhance the inflammatory response and lead to tissue damage. For instance, in asthma, a close relationship has been demonstrated between increased lung eosinophilia, asthma exacerbation, and loss of lung function. The use of an anti-IL-5 therapy in severe eosinophilic asthmatic patients is efficient to reduce exacerbations. However, anti-IL-5–treated patients still display a relatively high amount of functional lung tissue eosinophils, indicating that supplemental therapies are required to damper the eosinophil functions. Our recent published works suggest that compared to IL-5, IL-3 can more strongly and differentially affect eosinophil functions. In this review, we summarize our and other investigations that have compared the effects of the three β-chain receptor cytokines (IL-5, GM-CSF and IL-3) on eosinophil biology. We focus on how IL-3 differentially activates eosinophils compared to IL-5 or GM-CSF.


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