mTORC2 regulates multiple aspects of NKT-cell development and function.
Eur J Immunol
; 47(3): 516-526, 2017 03.
Article
em En
| MEDLINE
| ID: mdl-28078715
Invariant NKT (iNKT) cells bridge innate and adaptive immunity by rapidly secreting cytokines and lysing targets following TCR recognition of lipid antigens. Based on their ability to secrete IFN-γ, IL-4 and IL-17A, iNKT-cells are classified as NKT-1, NKT-2, and NKT-17 subsets, respectively. The molecular pathways regulating iNKT-cell fate are not fully defined. Recent studies implicate Rictor, a required component of mTORC2, in the development of select iNKT-cell subsets, however these reports are conflicting. To resolve these questions, we used Rictorfl/fl CD4cre+ mice and found that Rictor is required for NKT-17 cell development and normal iNKT-cell cytolytic function. Conversely, Rictor is not absolutely required for IL-4 and IFN-γ production as peripheral iNKT-cells make copious amounts of these cytokines. Overall iNKT-cell numbers are dramatically reduced in the absence of Rictor. We provide data indicating Rictor regulates cell survival as well as proliferation of developing and mature iNKT-cells. Thus, mTORC2 regulates multiple aspects of iNKT-cell development and function.
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Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Proteínas de Transporte
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Complexos Multiproteicos
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Células T Matadoras Naturais
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Serina-Treonina Quinases TOR
Limite:
Animals
Idioma:
En
Ano de publicação:
2017
Tipo de documento:
Article