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Title:
Fuel feeds function: energy metabolism and the T-cell response | Nature Reviews Immunology
Description:
Ligation of antigen receptors at the surface of lymphocytes initiates a transcriptional and translational response that is required for cellular proliferation and effector function. By contrast, co-stimulatory-molecule ligation contributes to the immune response by allowing the uptake and utilization of extracellular nutrients to provide energy for cellular proliferation and effector functions. Growth factors also potentiate the ability of lymphocytes to metabolically switch between resting and proliferative states. Lymphocytes that do not receive these signals fail to increase their metabolism to meet the higher bioenergetic demands of cell growth and are either deleted or rendered unresponsive to mitogenic signals. In this Review, we describe how T cells actively acquire metabolic substrates from their environment to meet these energy demands and respond appropriately to pathogens.
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nature portfolio mhc-class-i-dependent antigen presentation permissions reprints privacy policy long-term stationary-phase cultures 2-deoxy-d-glucose-induced metabolic stress advertising cancer research institute gene-knockout-mouse approach cell-cycle-related metabolic scientific reports social media nature genet nature rev nature immunol proto-oncogene kinase pim1 author information authors nature t-cell-dependent immune response research group pre-doctoral training grant akt/pkb signaling pathway c-myc-dependent pathway amp-activated protein kinase p53-dependent metabolic checkpoint cd8+ t-cell responses author correspondence stress-responsive kinase gcn2 serine/threonine kinase pim-2 serine/threonine kinase pim-1 neural precursor-cell expressed casitas b-lineage lymphoma internal ribosomal-entry sites ubiquitin-dependent proteasomal machinery maintaining t-cell memory mitochondrial loveβhate triangle rapamycin-independent signaling pathway suppress t-cell proliferation cd4/cd8 lineage decision ampk subfamily nuclear factor-ΞΊb activation regulatory cell development myeloid cell-mediated inflammation personal data cd8+ t-cell memory serine/threonine kinase inhibition nutrient-regulated protein kinases springerlink instant access antigen-presenting cells control t-cell response casey
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Ligation of antigen receptors at the surface of lymphocytes initiates a transcriptional and translational response that is required for cellular proliferation and effector function. By contrast, co-stimulatory-molecule ligation contributes to the immune response by allowing the uptake and utilization of extracellular nutrients to provide energy for cellular proliferation and effector functions. Growth factors also potentiate the ability of lymphocytes to metabolically switch between resting and proliferative states. Lymphocytes that do not receive these signals fail to increase their metabolism to meet the higher bioenergetic demands of cell growth and are either deleted or rendered unresponsive to mitogenic signals. In this Review, we describe how T cells actively acquire metabolic substrates from their environment to meet these energy demands and respond appropriately to pathogens.
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Ligation of antigen receptors at the surface of lymphocytes initiates a transcriptional and translational response that is required for cellular proliferation and effector function. By contrast, co-stimulatory-molecule ligation contributes to the immune response by allowing the uptake and utilization of extracellular nutrients to provide energy for cellular proliferation and effector functions. Growth factors also potentiate the ability of lymphocytes to metabolically switch between resting and proliferative states. Lymphocytes that do not receive these signals fail to increase their metabolism to meet the higher bioenergetic demands of cell growth and are either deleted or rendered unresponsive to mitogenic signals. In this Review, we describe how T cells actively acquire metabolic substrates from their environment to meet these energy demands and respond appropriately to pathogens.
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