The kinase mTOR regulates the differentiation of helper T cells through the selective activation of signaling by mTORC1 and mTORC2 View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2011-04

AUTHORS

Greg M Delgoffe, Kristen N Pollizzi, Adam T Waickman, Emily Heikamp, David J Meyers, Maureen R Horton, Bo Xiao, Paul F Worley, Jonathan D Powell

ABSTRACT

The kinase mTOR has emerged as an important regulator of the differentiation of helper T cells. Here we demonstrate that differentiation into the T(H)1 and T(H)17 subsets of helper T cells was selectively regulated by signaling from mTOR complex 1 (mTORC1) that was dependent on the small GTPase Rheb. Rheb-deficient T cells failed to generate T(H)1 and T(H)17 responses in vitro and in vivo and did not induce classical experimental autoimmune encephalomyelitis (EAE). However, they retained their ability to become T(H)2 cells. Alternatively, when mTORC2 signaling was deleted from T cells, they failed to generate T(H)2 cells in vitro and in vivo but preserved their ability to become T(H)1 and T(H)17 cells. Our data identify mechanisms by which two distinct signaling pathways downstream of mTOR regulate helper cell fate in different ways. These findings define a previously unknown paradigm that links T cell differentiation with selective metabolic signaling pathways. More... »

PAGES

295

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ni.2005

DOI

http://dx.doi.org/10.1038/ni.2005

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1035267474

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/21358638


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