Abstract
The conversion of naïve T cells into effector T cells is initiated by stimulation through the T-cell receptor (TCR). Upon activation, T cells undergo significant morphological and functional changes, putting new metabolic demands on the cell. Past research has identified the mammalian target of rapamycin (mTOR) as a critical regulator of cell metabolism, and the development of new genetic models has begun to reveal an important role for this pathway in the homeostasis and function of T lymphocytes. In this review, we focus on the most recent findings that demonstrate the ability of mTOR to regulate T-cell activation, CD8(+) memory cell formation and function, and helper T lineage differentiation. Furthermore, we highlight the importance of tight control of mTOR signaling by tuberous sclerosis complex 1 for T-cell homeostasis, and the regulation of mTOR signaling by diacylglycerol kinases and the RasGRP1-Ras-Erk1/2 pathway in the context of TCR signaling.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Cell Differentiation / immunology*
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DNA-Binding Proteins / immunology
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DNA-Binding Proteins / metabolism
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Diacylglycerol Kinase / immunology
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Diacylglycerol Kinase / metabolism
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Guanine Nucleotide Exchange Factors / immunology
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Guanine Nucleotide Exchange Factors / metabolism
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Humans
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Lymphocyte Activation / immunology*
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MAP Kinase Signaling System / immunology
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Mice
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Receptors, Antigen, T-Cell / immunology
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Signal Transduction / immunology*
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T-Lymphocytes / immunology*
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T-Lymphocytes / metabolism
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TOR Serine-Threonine Kinases / immunology*
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TOR Serine-Threonine Kinases / metabolism
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Tuberous Sclerosis Complex 1 Protein
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Tumor Suppressor Proteins / immunology
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Tumor Suppressor Proteins / metabolism
Substances
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DNA-Binding Proteins
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Guanine Nucleotide Exchange Factors
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RASGRP1 protein, human
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Receptors, Antigen, T-Cell
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Tsc1 protein, mouse
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Tuberous Sclerosis Complex 1 Protein
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Tumor Suppressor Proteins
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MTOR protein, human
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Diacylglycerol Kinase
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TOR Serine-Threonine Kinases