IL-21 receptor signaling is integral to the development of Th2 effector responses in vivo.

Détails

ID Serval
serval:BIB_FB884BF7AA60
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
IL-21 receptor signaling is integral to the development of Th2 effector responses in vivo.
Périodique
Blood
Auteur⸱e⸱s
Marsland B.J., Fröhlich A., Sonderegger I., Kurrer M., Hodge M.R., Harris N.L., Kopf M.
ISSN
0006-4971
Statut éditorial
Publié
Date de publication
2007
Peer-reviewed
Oui
Volume
109
Numéro
5
Pages
2023-2031
Langue
anglais
Résumé
Interleukin 21 (IL-21) is a member of the common gamma-chain family of cytokines, which influence a broad spectrum of immunologic responses. A number of studies have examined the function of IL-21, but its specific role in Th1/Th2-cell differentiation and related effector responses remains to be clarified. Thus, we generated IL-21R-deficient mice and have investigated the role of IL-21R signaling using a series of in vivo experimentally induced disease models. We first addressed the role of IL-21R signaling in Th2 immune responses by examining allergic airway inflammation, and Nippostrongylus brasiliensis and Heligmosomoides polygyrus antihelminth responses. In each of these systems, IL-21R signaling played a clear role in the development of Th2 responses. Comparatively, IL-21R signaling was not required for the containment of Leishmania major infection or the development of experimental autoimmune myocarditis, indicative of competent Th1 and Th17 responses, respectively. Adoptive transfer of T cells and analysis of IL-21R+/+/IL-21R-/- chimera mice revealed that IL-21R-signaling was central to Th2-cell survival or migration to peripheral tissues. Overall, our data show IL-21 plays a crucial role in supporting polarized Th2 responses in vivo, while appearing superfluous for Th1 and Th17 responses.
Mots-clé
Animals, Autoimmune Diseases/genetics, Autoimmune Diseases/immunology, Bronchial Diseases/genetics, Bronchial Diseases/immunology, Mice, Mice, Knockout, Myocarditis/genetics, Myocarditis/immunology, Nematospiroides dubius/immunology, Nippostrongylus/immunology, Receptors, Interleukin-21/deficiency, Receptors, Interleukin-21/genetics, Signal Transduction/immunology, Th2 Cells/immunology, Th2 Cells/metabolism
Pubmed
Web of science
Open Access
Oui
Création de la notice
18/01/2010 14:09
Dernière modification de la notice
20/08/2019 17:26
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