Evidence map›Paper›PMID 28555668›Full record

ArticleNature communications2017

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, David K Finlay

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
5.8field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

99 citing papers in PubMed, 176 citations in OpenAlex.

  1. Article
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  10. Metabolic Cross Talk in the Tumor Microenvironment.Cancer treatment and research · 2026
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  13. Article
  14. Metabolic Programming Drives Protective and Inflammatory Monocyte Fates in Viral Encephalitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  15. Review
  16. Review
  17. Dendritic cell maturation in cancer.Nature reviews. Cancer · 2025
    Review
  18. Review
  19. Article
  20. Review

39 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 3 countries.

Simon J LawlessSchool of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, 152-160 Pearce Street, Dublin 2, Ireland.
Nidhi Kedia-MehtaSchool of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, 152-160 Pearce Street, Dublin 2, Ireland.
Jessica F WallsSchool of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, 152-160 Pearce Street, Dublin 2, Ireland.
Ryan McGarrigleSchool of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, 152-160 Pearce Street, Dublin 2, Ireland.
Orla ConverySchool of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, 152-160 Pearce Street, Dublin 2, Ireland.
Linda V SinclairDivision of Cell Signalling and Immunology, School of Life Sciences, University of Dundee, Dow Street, Dundee DD1 5EH, Scotland, UK.ORCID 0000-0003-1248-7189
Maria N NavarroDepartamento Medicina/Universidad Autónoma de Madrid, Instituto Investigación Sanitaria/Hospital Universitario de la Princesa, C/Diego de Léon, 62, Madrid 28006, Spain.
James MurraySchool of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, 152-160 Pearce Street, Dublin 2, Ireland.
David K FinlaySchool of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, 152-160 Pearce Street, Dublin 2, Ireland.ORCID 0000-0003-2716-6679
Trinity College Dublin · IEHospital Universitario de La Princesa · ESUniversity of Dundee · GB

Funding

Wellcome Trust
6 · The paper itself

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.

Indexed as

AnimalsCD8-Positive T-LymphocytesCell DifferentiationCoculture TechniquesDendritic CellsGlucoseHypoxia-Inducible Factor 1, alpha SubunitInflammationInterferon-gammaLipopolysaccharidesMaleMiceMice, Inbred C57BLMicroscopy, ConfocalNitric OxideNitric Oxide Synthase Type IIGlucoseHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitInterferon-gammaLipopolysaccharidesNitric OxideNitric Oxide Synthase Type IINos2 protein, mouse

Identifiers

PMID28555668
PMCPMC5459989
OpenAlexW2619729916

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.