The mTOR kinase differentially regulates effector and regulatory T cell lineage commitment.

By Greg M. Delgoffe, T. Kole, Yan Zheng, Paul E. Zarek, K. Matthews, B. Xiao, P. Worley, S. Kozma, J. Powell. Immunity, 2009

1,280 citations recorded by the source corpus.

Subfields: Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/7400a9ce91109df2b95fc1d23a8f7763a9972eb4

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

In Oncology

Citations in the corpus

T cell metabolism drives immunity (2015, background): “…promoted the generation of FoxP3+ regulatory T (T reg) cells even in the presence of Th17-polarizing cytokines in vitro (Kopf et al., 2007), and genetic deletion of mTOR in T cells augmented production of T reg cells upon activation, but not Th1, Th2, or Th17 cells (Delgoffe et al., 2009).”
Alternative activation of macrophages: mechanism and functions. (2010, background): “The mTOR adaptor is an evolutionarily conserved member of the PI3K family that forms the core of distinct TORC1 and TORC2 signaling complexes, broadly responsible for the regulation of metabolism, growth, and proliferation (Delgoffe et al., 2009).”
The Glucose Transporter Glut1 is Selectively Essential for CD4 T Cell Activation and Effector Function (2014, neutral): “T cellspecific deletion of mTOR kinase to eliminate both mTORC1 and mTORC2 prevented generation of Teff but allowed establishment of functional Treg (Delgoffe et al., 2009).”
Inflammatory T cell responses rely on amino acid transporter ASCT2 facilitation of glutamine uptake and mTORC1 kinase activation (2014, positive): “for the generation of Th1 and Th17 cells, but not Treg cells (Delgoffe et al., 2009).”
HIF1α–dependent glycolytic pathway orchestrates a metabolic checkpoint for the differentiation of TH17 and Treg cells (2011, background): “Conversely, anergic T cells fail to up-regulate the machinery necessary to support increased metabolism (Delgoffe et al., 2009; Zheng et al., 2009), whereas memory cell formation requires a lower metabolic activity (Araki et al., 2009; Pearce et al., 2009).”
Regulatory T Cells: Mechanisms of Differentiation and Function (2012, background): “Furthermore, researchers reported that TORC2, which phosphorylates (Ser473) and activates Akt, represses Foxp3 induction and that TORC2 deficiency promoted Foxp3 induction under normal activation conditions (61).”
Glutamine: Metabolism and Immune Function, Supplementation and Clinical Translation (2018, background): “This pathway is also involved in the differentiation of CD4+ T-cell subsets since mTOR-deficient mice have a decrease in differentiation for effector T lymphocytes [130,131].”
The mTOR kinase determines effector versus memory cell fate of CD8+ T cells by regulating T-bet and Eomesodermin expression (2010, background): “Moreover, a recent report has implicated the requirement of mTOR kinase signaling in regulating effector versus regulatory cell lineage commitment in CD4 T cells (Delgoffe et al., 2009).”