Evidence map›Paper›PMID 31251396›Full record

ArticleClinical and experimental immunology2019

Type 2 diabetes is associated with the accumulation of senescent T cells.

E Y M Lau, E C Carroll, L A Callender, G A Hood, V Berryman, M Pattrick, S Finer, G A Hitman, G L Ackland, S M Henson

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical and experimental immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
–field-weighted citation impact
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

80 citing papers in PubMed.

  1. Trial
  2. Trial
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  5. Risk Factors for Secondary Immunodeficiency in the Aged.The journal of allergy and clinical immunology. In practice · 2026
    Review
  6. Article
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  8. Article
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  12. Article
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  15. Article
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  19. Article
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20 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

10 authors.

E Y M LauBarts and The London School of Medicine and Dentistry, William Harvey Research Institute, Queen Mary University of London, London, UK.
E C CarrollBarts and The London School of Medicine and Dentistry, William Harvey Research Institute, Queen Mary University of London, London, UK.
L A CallenderBarts and The London School of Medicine and Dentistry, William Harvey Research Institute, Queen Mary University of London, London, UK.
G A HoodBarts and The London School of Medicine and Dentistry, Blizard Institute, Queen Mary University of London, London, UK.
V BerrymanBarts Health NHS Trust, London, UK.
M PattrickBarts Health NHS Trust, London, UK.
S FinerBarts and The London School of Medicine and Dentistry, Blizard Institute, Queen Mary University of London, London, UK.
G A HitmanBarts and The London School of Medicine and Dentistry, Blizard Institute, Queen Mary University of London, London, UK.
G L AcklandBarts and The London School of Medicine and Dentistry, William Harvey Research Institute, Queen Mary University of London, London, UK.
S M HensonBarts and The London School of Medicine and Dentistry, William Harvey Research Institute, Queen Mary University of London, London, UK.ORCID 0000-0003-1893-4912

Funding

British Heart Foundation FS/15/69/32043Cancer Research UK C16420/A18066Wellcome Trust
6 · The paper itself

Abstract

Type 2 diabetes is a global health priority, given that it is driven, in part, by an ageing population, the role of immune senescence has been overlooked. This is surprising, as the functional impairments of senescent T cells show strong similarities to patients with hyperglycaemia. Immune senescence is typified by alterations in T cell memory, such as the accumulation of highly differentiated end-stage memory T cells, as well as a constitutive low-grade inflammation, which drives further immune differentiation. We show here in a preliminary study that people living with type 2 diabetes have a higher circulating volume of senescent T cells accompanied with a higher level of systemic inflammation. This inflammatory environment drives the expression of a unique array of chemokine receptors on senescent T cells, most notably C-X-C motif chemokine receptor type 2. However, this increased expression of migratory markers does not translate to improved extravasation owing to a lack of glucose uptake by the T cells. Our results therefore demonstrate that the presence of senescent T cells has a detrimental impact on immune function during type 2 diabetes.

Indexed as

AgedAgingCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell MovementCellular SenescenceDiabetes Mellitus, Type 2FemaleGlucoseHumansImmunologic MemoryInflammationInsulin ResistanceLymphocyte CountMaleMiddle AgedGlucoseReceptors, ChemokineageinginflammationsenescentT celltype 2 diabetes

Identifiers

PMID31251396
PMCPMC6642873

What OpenQuestion holds

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Registered trials

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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.