Glucose represses dendritic cell-induced T cell responses

Simon J. Lawless, Nidhi Kedia-Mehta, Jessica F. Walls, Ryan McGarrigle, Orla Convery, Linda V. Sinclair, Maria N. Navarro, James Murray and David K. Finlay ()
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Simon J. Lawless: School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin
Nidhi Kedia-Mehta: School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin
Jessica F. Walls: School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin
Ryan McGarrigle: School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin
Orla Convery: School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin
Linda V. Sinclair: School of Life Sciences, University of Dundee
Maria N. Navarro: Instituto Investigación Sanitaria/Hospital Universitario de la Princesa
James Murray: School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin
David K. Finlay: School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin

Nature Communications, 2017, vol. 8, issue 1, 1-14

Abstract: 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.

Date: 2017
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DOI: 10.1038/ncomms15620

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