Evidence map›Paper›PMID 29166588›Full record

ArticleImmunity2017

Regulatory T Cell Migration Is Dependent on Glucokinase-Mediated Glycolysis.

Madhav Kishore, Kenneth C P Cheung, Hongmei Fu, Fabrizia Bonacina, Guosu Wang, David Coe, Eleanor J Ward, Alessandra Colamatteo, Maryam Jangani, Andrea Baragetti and 10 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 167 papers.

0numbers the graph read from it
0cells of the map it votes in
167citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

167 citing papers in PubMed, 273 citations in OpenAlex.

  1. Trial
  2. Review
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  8. Review
  9. Regulatory T cells in cancer and inflammation.Signal transduction and targeted therapy · 2026
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. The pyruvate branch point controls lymphoid cancer cell dissemination.bioRxiv : the preprint server for biology · 2026
    Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 9 institutions in 3 countries.

Madhav KishoreWilliam Harvey Research Institute, Queen Mary University of London, London EC1M6BQ, UK.
Kenneth C P CheungWilliam Harvey Research Institute, Queen Mary University of London, London EC1M6BQ, UK.
Hongmei FuWilliam Harvey Research Institute, Queen Mary University of London, London EC1M6BQ, UK.
Fabrizia BonacinaDepartment of Pharmacological and Biomolecular Sciences, University of Milan, Milan 20133, Italy.
Guosu WangWilliam Harvey Research Institute, Queen Mary University of London, London EC1M6BQ, UK.
David CoeWilliam Harvey Research Institute, Queen Mary University of London, London EC1M6BQ, UK.
Eleanor J WardWilliam Harvey Research Institute, Queen Mary University of London, London EC1M6BQ, UK.
Alessandra ColamatteoIstituto per l'Endocrinologia e l'Oncologia Sperimentale, Consiglio Nazionale delle Ricerche (IEOS-CNR), Naples 80131, Italy.
Maryam JanganiWilliam Harvey Research Institute, Queen Mary University of London, London EC1M6BQ, UK.
Andrea BaragettiDepartment of Pharmacological and Biomolecular Sciences, University of Milan, Milan 20133, Italy.
Giuseppe MatareseIstituto per l'Endocrinologia e l'Oncologia Sperimentale, Consiglio Nazionale delle Ricerche (IEOS-CNR), Naples 80131, Italy; Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università di Napoli "Federico II," Naples 80131, Italy.
David M SmithDiscovery Sciences, Innovative Medicines and Early Development Biotech Unit, AstraZeneca, Cambridge, Cambridgeshire CB40WG, UK.
Robert HaasWilliam Harvey Research Institute, Queen Mary University of London, London EC1M6BQ, UK.
Claudio MauroWilliam Harvey Research Institute, Queen Mary University of London, London EC1M6BQ, UK.
David C WraithInstitute of Immunology and Immunotherapy, University of Birmingham, Birmingham B15 2TT, UK.
Klaus OkkenhaugLaboratory of Lymphocyte Signalling and Development, Babraham Institute, Cambridge CB22 3AT, UK.
Alberico L CatapanoDepartment of Pharmacological and Biomolecular Sciences, University of Milan, Milan 20133, Italy; IRCCS Multimedica Hospital, Milan 20138, Italy.
Veronica De RosaIstituto per l'Endocrinologia e l'Oncologia Sperimentale, Consiglio Nazionale delle Ricerche (IEOS-CNR), Naples 80131, Italy.
Giuseppe D NorataDepartment of Pharmacological and Biomolecular Sciences, University of Milan, Milan 20133, Italy; School of Biomedical Sciences, Curtin Health Innovation Research Institute, Curtin University, Perth, WA 6102, Australia.
Federica M Marelli-BergWilliam Harvey Research Institute, Queen Mary University of London, London EC1M6BQ, UK. Electronic address: f.marelli-berg@qmul.ac.uk.
Queen Mary University of London · GBWilliam Harvey Research Institute · GBUniversity of Milan · ITNational Research Council · ITAstraZeneca (United Kingdom) · GBBabraham Institute · GBInstitute for Experimental Endocrinology and Oncology · ITMultiMedica · ITUniversity of Birmingham · GB

Funding

Biotechnology and Biological Sciences Research Council BBS/E/B/000C0407Biotechnology and Biological Sciences Research Council BBS/E/B/000C0409British Heart Foundation CH/15/2/32064British Heart Foundation FS/11/64/28945British Heart Foundation FS/12/38/29640British Heart Foundation PG/15/105/31906British Heart Foundation RG/14/2/30616Medical Research Council MR/P021220/1
6 · The paper itself

Abstract

Migration of activated regulatory T (Treg) cells to inflamed tissue is crucial for their immune-modulatory function. While metabolic reprogramming during Treg cell differentiation has been extensively studied, the bioenergetics of Treg cell trafficking remains undefined. We have investigated the metabolic demands of migrating Treg cells in vitro and in vivo. We show that glycolysis was instrumental for their migration and was initiated by pro-migratory stimuli via a PI3K-mTORC2-mediated pathway culminating in induction of the enzyme glucokinase (GCK). Subsequently, GCK promoted cytoskeletal rearrangements by associating with actin. Treg cells lacking this pathway were functionally suppressive but failed to migrate to skin allografts and inhibit rejection. Similarly, human carriers of a loss-of-function GCK regulatory protein gene-leading to increased GCK activity-had reduced numbers of circulating Treg cells. These cells displayed enhanced migratory activity but similar suppressive function, while conventional T cells were unaffected. Thus, GCK-dependent glycolysis regulates Treg cell migration.

Indexed as

GlycolysisAdaptor Proteins, Signal TransducingAnimalsCD28 AntigensCells, CulturedCTLA-4 AntigenGlucokinaseHumansMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2MiceMice, Inbred StrainsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktT-Lymphocytes, RegulatoryAdaptor Proteins, Signal TransducingCD28 AntigensCTLA-4 AntigenGCKR protein, humanGlucokinaseMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktCD28CTLA-4glycolysismetabolismmigrationmTORregulatory T cells

Identifiers

PMID29166588
PMCPMC5714502
OpenAlexW2769148407

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.