Evidence map›Paper›PMID 26746193›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

CD46 Activation Regulates miR-150-Mediated Control of GLUT1 Expression and Cytokine Secretion in Human CD4+ T Cells.

Ben C King, Jonathan L S Esguerra, Ewelina Golec, Lena Eliasson, Claudia Kemper, Anna M Blom

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Noncoding RNAs: the shot callers in tumor immune escape.Signal transduction and targeted therapy · 2020
    Review
  16. Review
  17. Article
  18. Non-Coding RNAs in CD4Frontiers in immunology · 2020
    Review
  19. Review
  20. Article
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

6 authors at 2 institutions in 2 countries.

Ben C KingSection of Medical Protein Chemistry, Department of Translational Medicine, Lund University, 205-02 Malmö, Sweden;
Jonathan L S EsguerraIslet Cell Exocytosis Unit, Lund University Diabetes Center, Department of Clinical Sciences Malmö, Lund University, 205-02 Malmö, Sweden; and.ORCID http://orcid.org/0000-0001-8454-6606
Ewelina GolecSection of Medical Protein Chemistry, Department of Translational Medicine, Lund University, 205-02 Malmö, Sweden;ORCID http://orcid.org/0000-0002-3062-4020
Lena EliassonIslet Cell Exocytosis Unit, Lund University Diabetes Center, Department of Clinical Sciences Malmö, Lund University, 205-02 Malmö, Sweden; and.ORCID http://orcid.org/0000-0002-6467-5029
Claudia KemperDivision of Transplant Immunology and Mucosal Biology, Medical Research Council Centre for Transplantation, King's College London, Guy's Hospital, London SE1 9RT, United Kingdom.
Anna M BlomSection of Medical Protein Chemistry, Department of Translational Medicine, Lund University, 205-02 Malmö, Sweden; Anna.blom@med.lu.se.ORCID http://orcid.org/0000-0002-1348-1734
Lund University · SEGuy's Hospital · GB

Funding

Medical Research Council G1002165Medical Research Council MR/J006742/1Wellcome Trust
6 · The paper itself

Abstract

CD46 is a cell surface complement inhibitor widely expressed in human tissues, in contrast to mice, where expression is limited to the testes. In humans, it has been identified as an important T cell costimulatory receptor, and patients deficient in CD46 or its endogenous ligands are unable to mount effective Th1 T cell responses. Stimulation of human CD4(+) T cells with CD3 and CD46 also leads to the differentiation of a "switched" Th1 population, which shuts down IFN-γ secretion and upregulates IL-10 and is thought to be important for negative feedback regulation of the Th1 response. In the present study, we show that CD46 costimulation leads to amplified microRNA (miR) expression changes in human CD4(+) T cells, with associated increases in activation more potent than those mediated by the "classic" costimulator CD28. Blockade of cell surface CD46 inhibited CD28-mediated costimulation, identifying autocrine CD46 signaling as downstream of CD28. We also identify a downregulation of miR-150 in CD46-costimulated T cells and identify the glucose transporter 1 encoding transcript SLC2A1 as a target of miR-150 regulation, connecting miR-150 with modulation of glucose uptake. We also investigated microRNA expression profiles of CD46-induced switched IL-10-secreting Th1 T cells and found increased expression of miR-150, compared with IFN-γ-secreting Th1 cells. Knockdown of miR-150 led to a reduction in IL-10 but not IFN-γ. CD46 therefore controls both Th1 activation and regulation via a miR-150-dependent mechanism.

Indexed as

CD4-Positive T-LymphocytesCell SeparationCytokinesGene Expression RegulationGlucose Transporter Type 1HumansImmunoblottingLymphocyte ActivationMembrane Cofactor ProteinMicroRNAsOligonucleotide Array Sequence AnalysisPolymerase Chain ReactionTh1 CellsCD46 protein, humanCytokinesGlucose Transporter Type 1Membrane Cofactor ProteinMicroRNAsMIR150, human

Identifiers

PMID26746193
PMCPMC4745132
OpenAlexW2257705883

What OpenQuestion holds

Textmetadata
LicenceTDM
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.