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mTOR, metabolism, and the regulation of T-cell differentiation and function

Authors

  • Adam T. Waickman,

    1. Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA
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  • Jonathan D. Powell

    Corresponding author
    • Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA
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Correspondence to:

Jonathan D. Powell

Department of Oncology

Sidney Kimmel Comprehensive Cancer Center

Johns Hopkins University School of Medicine

1650 Orleans Street, Room 443

Baltimore, MD 21231, USA

Tel.: +1 410 532 1736

Fax: +1 410 614 9705

e-mail: poweljo@jhmi.edu

Summary

Upon antigen recognition, naive T cells undergo rapid expansion and activation. The energy requirements for this expansion are formidable, and T-cell activation is accompanied by dramatic changes in cellular metabolism. Furthermore, the outcome of antigen engagement is guided by multiple cues derived from the immune microenvironment. Mammalian target of rapamycin (mTOR) is emerging as a central integrator of these signals playing a critical role in driving T-cell differentiation and function. Indeed, multiple metabolic programs are controlled by mTOR signaling. In this review, we discuss the role of mTOR in regulating metabolism and how these pathways intersect with the ability of mTOR to integrate cues that guide the outcome of T-cell receptor engagement.

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