RapamycinFungusV1, Main, Exploration, bibRecord, 000B48

Antigen-Specific Immune Modulation Targets mTORC1 Function To Drive Chemokine Receptor-Mediated T Cell Tolerance.

Identifieur interne : 000B48 ( Main/Exploration ); précédent : 000B47; suivant : 000B49

Antigen-Specific Immune Modulation Targets mTORC1 Function To Drive Chemokine Receptor-Mediated T Cell Tolerance.

Auteurs : Weirong Chen [États-Unis] ; Xiaoxiao Wan [États-Unis] ; Tobechukwu K. Ukah [États-Unis] ; Mindy M. Miller [États-Unis] ; Subhasis Barik [États-Unis] ; Alexis N. Cattin-Roy [États-Unis] ; Habib Zaghouani [États-Unis]

Source :

Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2016.

RBID : pubmed:27671108

Descripteurs français

English descriptors

KwdEn :
- Animals (MeSH), Antigens (immunology), Autoimmunity (MeSH), B7-H1 Antigen (metabolism), Cells, Cultured (MeSH), Diabetes Mellitus, Type 1 (immunology), Diabetes Mellitus, Type 1 (therapy), Immune Tolerance (MeSH), Immunomodulation (MeSH), Mechanistic Target of Rapamycin Complex 1 (MeSH), Mice (MeSH), Mice, Inbred NOD (MeSH), Multiprotein Complexes (immunology), Programmed Cell Death 1 Receptor (metabolism), Receptors, CXCR3 (metabolism), Signal Transduction (MeSH), T-Lymphocytes (immunology), TOR Serine-Threonine Kinases (immunology).
MESH :
- chemical , immunology : Antigens, Multiprotein Complexes, TOR Serine-Threonine Kinases.
- chemical , metabolism : B7-H1 Antigen, Programmed Cell Death 1 Receptor, Receptors, CXCR3.
- immunology : Diabetes Mellitus, Type 1, T-Lymphocytes.
- therapy : Diabetes Mellitus, Type 1.
- Animals, Autoimmunity, Cells, Cultured, Immune Tolerance, Immunomodulation, Mechanistic Target of Rapamycin Complex 1, Mice, Mice, Inbred NOD, Signal Transduction.

Abstract

To contain autoimmunity, pathogenic T cells must be eliminated or diverted from reaching the target organ. Recently, we defined a novel form of T cell tolerance whereby treatment with Ag downregulates expression of the chemokine receptor CXCR3 and prevents diabetogenic Th1 cells from reaching the pancreas, leading to suppression of type 1 diabetes (T1D). This report defines the signaling events underlying Ag-induced chemokine receptor-mediated tolerance. Specifically, we show that the mammalian target of rapamycin complex 1 (mTORC1) is a major target for induction of CXCR3 downregulation and crippling of Th1 cells. Indeed, Ag administration induces upregulation of programmed death-ligand 1 on dendritic cells in a T cell-dependent manner. In return, programmed death-ligand 1 interacts with the constitutively expressed programmed death-1 on the target T cells and stimulates docking of Src homology 2 domain-containing tyrosine phosphatase 2 phosphatase to the cytoplasmic tail of programmed death-1. Active Src homology 2 domain-containing tyrosine phosphatase 2 impairs the signaling function of the PI3K/protein kinase B (AKT) pathway, leading to functional defect of mTORC1, downregulation of CXCR3 expression, and suppression of T1D. Thus, mTORC1 component of the metabolic pathway serves as a target for chemokine receptor-mediated T cell tolerance and suppression of T1D.

DOI: 10.4049/jimmunol.1601032
PubMed: 27671108
PubMed Central: PMC5101142

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<term>Récepteur-1 de mort cellulaire programmée (métabolisme)</term>
<term>Récepteurs CXCR3 (métabolisme)</term>
<term>Souris (MeSH)</term>
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<term>TOR Serine-Threonine Kinases</term>
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<term>Diabète de type 1</term>
<term>Lymphocytes T</term>
<term>Sérine-thréonine kinases TOR</term>
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<front><div type="abstract" xml:lang="en">To contain autoimmunity, pathogenic T cells must be eliminated or diverted from reaching the target organ. Recently, we defined a novel form of T cell tolerance whereby treatment with Ag downregulates expression of the chemokine receptor CXCR3 and prevents diabetogenic Th1 cells from reaching the pancreas, leading to suppression of type 1 diabetes (T1D). This report defines the signaling events underlying Ag-induced chemokine receptor-mediated tolerance. Specifically, we show that the mammalian target of rapamycin complex 1 (mTORC1) is a major target for induction of CXCR3 downregulation and crippling of Th1 cells. Indeed, Ag administration induces upregulation of programmed death-ligand 1 on dendritic cells in a T cell-dependent manner. In return, programmed death-ligand 1 interacts with the constitutively expressed programmed death-1 on the target T cells and stimulates docking of Src homology 2 domain-containing tyrosine phosphatase 2 phosphatase to the cytoplasmic tail of programmed death-1. Active Src homology 2 domain-containing tyrosine phosphatase 2 impairs the signaling function of the PI3K/protein kinase B (AKT) pathway, leading to functional defect of mTORC1, downregulation of CXCR3 expression, and suppression of T1D. Thus, mTORC1 component of the metabolic pathway serves as a target for chemokine receptor-mediated T cell tolerance and suppression of T1D.</div>
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<Abstract><AbstractText>To contain autoimmunity, pathogenic T cells must be eliminated or diverted from reaching the target organ. Recently, we defined a novel form of T cell tolerance whereby treatment with Ag downregulates expression of the chemokine receptor CXCR3 and prevents diabetogenic Th1 cells from reaching the pancreas, leading to suppression of type 1 diabetes (T1D). This report defines the signaling events underlying Ag-induced chemokine receptor-mediated tolerance. Specifically, we show that the mammalian target of rapamycin complex 1 (mTORC1) is a major target for induction of CXCR3 downregulation and crippling of Th1 cells. Indeed, Ag administration induces upregulation of programmed death-ligand 1 on dendritic cells in a T cell-dependent manner. In return, programmed death-ligand 1 interacts with the constitutively expressed programmed death-1 on the target T cells and stimulates docking of Src homology 2 domain-containing tyrosine phosphatase 2 phosphatase to the cytoplasmic tail of programmed death-1. Active Src homology 2 domain-containing tyrosine phosphatase 2 impairs the signaling function of the PI3K/protein kinase B (AKT) pathway, leading to functional defect of mTORC1, downregulation of CXCR3 expression, and suppression of T1D. Thus, mTORC1 component of the metabolic pathway serves as a target for chemokine receptor-mediated T cell tolerance and suppression of T1D.</AbstractText>
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Antigen-Specific Immune Modulation Targets mTORC1 Function To Drive Chemokine Receptor-Mediated T Cell Tolerance.

Antigen-Specific Immune Modulation Targets mTORC1 Function To Drive Chemokine Receptor-Mediated T Cell Tolerance.

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