Amino Acids License Kinase mTORC1 Activity and Treg Cell Function via Small G Proteins Rag and Rheb

Regulatory T (Treg) cells are critical mediators of immune tolerance whose activity depends upon T cell receptor (TCR) and mTORC1 kinase signaling, but the mechanisms that dictate functional activation of these pathways are incompletely understood. Here, we showed that amino acids license Treg cell...

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Vydané v:Immunity (Cambridge, Mass.) Ročník 51; číslo 6; s. 1012
Hlavní autori: Shi, Hao, Chapman, Nicole M, Wen, Jing, Guy, Cliff, Long, Lingyun, Dhungana, Yogesh, Rankin, Sherri, Pelletier, Stephane, Vogel, Peter, Wang, Hong, Peng, Junmin, Guan, Kun-Liang, Chi, Hongbo
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States 17.12.2019
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Abstract Regulatory T (Treg) cells are critical mediators of immune tolerance whose activity depends upon T cell receptor (TCR) and mTORC1 kinase signaling, but the mechanisms that dictate functional activation of these pathways are incompletely understood. Here, we showed that amino acids license Treg cell function by priming and sustaining TCR-induced mTORC1 activity. mTORC1 activation was induced by amino acids, especially arginine and leucine, accompanied by the dynamic lysosomal localization of the mTOR and Tsc complexes. Rag and Rheb GTPases were central regulators of amino acid-dependent mTORC1 activation in effector Treg (eTreg) cells. Mice bearing RagA-RagB- or Rheb1-Rheb2-deficient Treg cells developed a fatal autoimmune disease and had reduced eTreg cell accumulation and function. RagA-RagB regulated mitochondrial and lysosomal fitness, while Rheb1-Rheb2 enforced eTreg cell suppressive gene signature. Together, these findings reveal a crucial requirement of amino acid signaling for licensing and sustaining mTORC1 activation and functional programming of Treg cells.
AbstractList Regulatory T (Treg) cells are critical mediators of immune tolerance whose activity depends upon T cell receptor (TCR) and mTORC1 kinase signaling, but the mechanisms that dictate functional activation of these pathways are incompletely understood. Here, we showed that amino acids license Treg cell function by priming and sustaining TCR-induced mTORC1 activity. mTORC1 activation was induced by amino acids, especially arginine and leucine, accompanied by the dynamic lysosomal localization of the mTOR and Tsc complexes. Rag and Rheb GTPases were central regulators of amino acid-dependent mTORC1 activation in effector Treg (eTreg) cells. Mice bearing RagA-RagB- or Rheb1-Rheb2-deficient Treg cells developed a fatal autoimmune disease and had reduced eTreg cell accumulation and function. RagA-RagB regulated mitochondrial and lysosomal fitness, while Rheb1-Rheb2 enforced eTreg cell suppressive gene signature. Together, these findings reveal a crucial requirement of amino acid signaling for licensing and sustaining mTORC1 activation and functional programming of Treg cells.
Regulatory T (Treg) cells are critical mediators of immune tolerance whose activity depends upon T cell receptor (TCR) and mTORC1 kinase signaling, but the mechanisms that dictate functional activation of these pathways are incompletely understood. Here, we showed that amino acids license Treg cell function by priming and sustaining TCR-induced mTORC1 activity. mTORC1 activation was induced by amino acids, especially arginine and leucine, accompanied by the dynamic lysosomal localization of the mTOR and Tsc complexes. Rag and Rheb GTPases were central regulators of amino acid-dependent mTORC1 activation in effector Treg (eTreg) cells. Mice bearing RagA-RagB- or Rheb1-Rheb2-deficient Treg cells developed a fatal autoimmune disease and had reduced eTreg cell accumulation and function. RagA-RagB regulated mitochondrial and lysosomal fitness, while Rheb1-Rheb2 enforced eTreg cell suppressive gene signature. Together, these findings reveal a crucial requirement of amino acid signaling for licensing and sustaining mTORC1 activation and functional programming of Treg cells.Regulatory T (Treg) cells are critical mediators of immune tolerance whose activity depends upon T cell receptor (TCR) and mTORC1 kinase signaling, but the mechanisms that dictate functional activation of these pathways are incompletely understood. Here, we showed that amino acids license Treg cell function by priming and sustaining TCR-induced mTORC1 activity. mTORC1 activation was induced by amino acids, especially arginine and leucine, accompanied by the dynamic lysosomal localization of the mTOR and Tsc complexes. Rag and Rheb GTPases were central regulators of amino acid-dependent mTORC1 activation in effector Treg (eTreg) cells. Mice bearing RagA-RagB- or Rheb1-Rheb2-deficient Treg cells developed a fatal autoimmune disease and had reduced eTreg cell accumulation and function. RagA-RagB regulated mitochondrial and lysosomal fitness, while Rheb1-Rheb2 enforced eTreg cell suppressive gene signature. Together, these findings reveal a crucial requirement of amino acid signaling for licensing and sustaining mTORC1 activation and functional programming of Treg cells.
Author Guy, Cliff
Vogel, Peter
Long, Lingyun
Peng, Junmin
Wen, Jing
Chi, Hongbo
Pelletier, Stephane
Chapman, Nicole M
Wang, Hong
Dhungana, Yogesh
Rankin, Sherri
Guan, Kun-Liang
Shi, Hao
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  organization: Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA
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  organization: Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA
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  organization: Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA
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  organization: Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA
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  surname: Wang
  fullname: Wang, Hong
  organization: Department of Structural Biology and Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA; Center for Proteomics and Metabolomics, St. Jude Children's Research Hospital, Memphis, TN 38105, USA
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  organization: Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. Electronic address: hongbo.chi@stjude.org
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Keywords autoimmunity
Rheb
eTreg cells
amino acids
mTOR
Treg cells
metabolism
RagB
RagA
Language English
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Snippet Regulatory T (Treg) cells are critical mediators of immune tolerance whose activity depends upon T cell receptor (TCR) and mTORC1 kinase signaling, but the...
Regulatory T (Treg) cells are critical mediators of immune tolerance whose activity depends upon T cell receptor (TCR) and mTORC1 kinase signaling, but the...
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SubjectTerms Animals
Arginine - metabolism
Cell Cycle
Cell Differentiation - physiology
Cell Line
Humans
Immune Tolerance - immunology
Leucine - metabolism
Lymphocyte Activation - immunology
Mechanistic Target of Rapamycin Complex 1 - metabolism
Mice
Mice, Inbred C57BL
Mice, Knockout
Monomeric GTP-Binding Proteins - genetics
Monomeric GTP-Binding Proteins - metabolism
Ras Homolog Enriched in Brain Protein - genetics
Ras Homolog Enriched in Brain Protein - metabolism
Receptors, Antigen, T-Cell - immunology
T-Lymphocytes, Regulatory - cytology
T-Lymphocytes, Regulatory - immunology
Title Amino Acids License Kinase mTORC1 Activity and Treg Cell Function via Small G Proteins Rag and Rheb
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