Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12530/39438
Title: Glucose represses dendritic cell-induced T cell responses.
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Issue Date: 2017
Citation: Nat Commun.2017 05;(8):15620
Abstract: Glucose and glycolysis are important for the proinflammatory functions of many immune cells, and depletion of glucose in pathological microenvironments is associated with defective immune responses. Here we show a contrasting function for glucose in dendritic cells (DCs), as glucose represses the proinflammatory output of LPS-stimulated DCs and inhibits DC-induced T-cell responses. A glucose-sensitive signal transduction circuit involving the mTOR complex 1 (mTORC1), HIF1α and inducible nitric oxide synthase (iNOS) coordinates DC metabolism and function to limit DC-stimulated T-cell responses. When multiple T cells interact with a DC, they compete for nutrients, which can limit glucose availability to the DCs. In such DCs, glucose-dependent signalling is inhibited, altering DC outputs and enhancing T-cell responses. These data reveal a mechanism by which T cells regulate the DC microenvironment to control DC-induced T-cell responses and indicate that glucose is an important signal for shaping immune responses.
PMID: 28555668
URI: https://hdl.handle.net/20.500.12530/39438
Rights: openAccess
Appears in Collections:Fundaciones e Institutos de Investigación > IIS H. U. La Princesa > Artículos

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