Essential Mechanisms of Differential ...
Type de document :
Article dans une revue scientifique: Article de synthèse/Review paper
PMID :
URL permanente :
Titre :
Essential Mechanisms of Differential Activation of Eosinophils by IL-3 Compared to GM-CSF and IL-5.
Auteur(s) :
Esnault, Stéphane [Auteur]
University of Wisconsin School of Medicine and Public Health
Kelly, Elizabeth A [Auteur]
University of Wisconsin School of Medicine and Public Health
University of Wisconsin School of Medicine and Public Health
Kelly, Elizabeth A [Auteur]
University of Wisconsin School of Medicine and Public Health
Titre de la revue :
Critical Reviews in Immunology
Nom court de la revue :
Crit Rev Immunol
Numéro :
36
Pagination :
429-444
Date de publication :
2016-09-05
ISSN :
1040-8401
Mot(s)-clé(s) en anglais :
Animals
Antibodies, Blocking
Asthma
Cell Differentiation
Eosinophilia
Eosinophils
Granulocyte-Macrophage Colony-Stimulating Factor
Humans
Immunotherapy
Interleukin-3
Interleukin-5
Antibodies, Blocking
Asthma
Cell Differentiation
Eosinophilia
Eosinophils
Granulocyte-Macrophage Colony-Stimulating Factor
Humans
Immunotherapy
Interleukin-3
Interleukin-5
Discipline(s) HAL :
Sciences du Vivant [q-bio]
Résumé en anglais : [en]
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 ...
Lire la suite >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.Lire moins >
Lire la suite >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.Lire moins >
Langue :
Anglais
Comité de lecture :
Oui
Audience :
Internationale
Vulgarisation :
Non
Établissement(s) :
Université de Lille
Inserm
CHU Lille
Inserm
CHU Lille
Collections :
Date de dépôt :
2023-10-23T15:29:37Z
2024-03-16T08:39:40Z
2024-03-16T08:39:40Z
Fichiers
- Essential mechanisms of differential activation 2016.pdf
- Version finale acceptée pour publication (postprint)
- Accès libre
- Accéder au document