Mammalian target of rapamycin complex 1 orchestrates invariant NKT cell differentiation and effector function.

Détails

ID Serval
serval:BIB_99C0A8A031A8
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Mammalian target of rapamycin complex 1 orchestrates invariant NKT cell differentiation and effector function.
Périodique
Journal of Immunology
Auteur(s)
Zhang L., Tschumi B.O., Corgnac S., Rüegg M.A., Hall M.N., Mach J.P., Romero P., Donda A.
ISSN
1550-6606 (Electronic)
ISSN-L
0022-1767
Statut éditorial
Publié
Date de publication
2014
Volume
193
Numéro
4
Pages
1759-1765
Langue
anglais
Résumé
Invariant NKT (iNKT) cells play critical roles in bridging innate and adaptive immunity. The Raptor containing mTOR complex 1 (mTORC1) has been well documented to control peripheral CD4 or CD8 T cell effector or memory differentiation. However, the role of mTORC1 in iNKT cell development and function remains largely unknown. By using mice with T cell-restricted deletion of Raptor, we show that mTORC1 is selectively required for iNKT but not for conventional T cell development. Indeed, Raptor-deficient iNKT cells are mostly blocked at thymic stage 1-2, resulting in a dramatic decrease of terminal differentiation into stage 3 and severe reduction of peripheral iNKT cells. Moreover, residual iNKT cells in Raptor knockout mice are impaired in their rapid cytokine production upon αGalcer challenge. Bone marrow chimera studies demonstrate that mTORC1 controls iNKT differentiation in a cell-intrinsic manner. Collectively, our data provide the genetic evidence that iNKT cell development and effector functions are under the control of mTORC1 signaling.
Pubmed
Web of science
Open Access
Oui
Création de la notice
26/09/2014 8:26
Dernière modification de la notice
20/08/2019 15:01
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