Evidence map›Paper›PMID 26518995›Full record

ArticleEuropean journal of immunology2016

Coincident diabetes mellitus modulates Th1-, Th2-, and Th17-cell responses in latent tuberculosis in an IL-10- and TGF-β-dependent manner.

Nathella Pavan Kumar, Kadar Moideen, Parakkal Jovvian George, Chandrakumar Dolla, Paul Kumaran, Subash Babu

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in European journal of immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 3 pooled it
1.9field-weighted citation impact, top 15% 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

28 citing papers in PubMed, 3 syntheses or guidelines pooled it, 53 citations in OpenAlex.

  1. Pooled it
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  9. ImpairedFrontiers in immunology · 2024
    Article
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  13. Observational
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  15. Impact of diabetes mellitus on immunity to latent tuberculosis infection.Frontiers in clinical diabetes and healthcare · 2023
    Review
  16. Article
  17. Review
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  19. Article
  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 1 country.

Nathella Pavan KumarNational Institutes of Health-NIRT-International Center for Excellence in Research, Chennai, India.
Kadar MoideenNational Institutes of Health-NIRT-International Center for Excellence in Research, Chennai, India.
Parakkal Jovvian GeorgeNational Institutes of Health-NIRT-International Center for Excellence in Research, Chennai, India.
Chandrakumar DollaNational Institute for Research in Tuberculosis, Chennai, India.
Paul KumaranNational Institute for Research in Tuberculosis, Chennai, India.
Subash BabuNational Institutes of Health-NIRT-International Center for Excellence in Research, Chennai, India.
International Centers for Excellence in Research · INNational Institute of Research in Tuberculosis · IN

Funding

India International Center for Excellence in ResearchZIAAI001065 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI NUTMAN, THOMAS · 2009 to 2025
$19.0M
Intramural NIH HHS Z99 AI999999
6 · The paper itself

Abstract

Type 2 diabetes mellitus (DM) is a risk factor for the development of active tuberculosis (TB), although its role in the TB-induced responses in latent TB (LTB) is not well understood. Since Th1, Th2, and Th17 responses are important in immunity to LTB, we postulated that coincident DM could alter the function of these CD4(+) T-cell subsets. To this end, we examined mycobacteria-induced immune responses in the whole blood of individuals with LTB-DM and compared them with responses of individuals without DM (LTB-NDM). T-cell responses from LTB-DM are characterized by diminished frequencies of mono- and dual-functional CD4(+) Th1, Th2, and Th17 cells at baseline and following stimulation with mycobacterial antigens-purified protein derivative, early secreted antigen-6, and culture filtrate protein-10. This modulation was at least partially dependent on IL-10 and TGF-β, since neutralization of either cytokine resulted in significantly increased frequencies of Th1 and Th2 cells but not Th17 cells in LTB-DM but not LTB individuals. LTB-DM is therefore characterized by diminished frequencies of Th1, Th2, and Th17 cells, indicating that DM alters the immune response in latent TB leading to a suboptimal induction of protective CD4(+) T-cell responses, thereby providing a potential mechanism for increased susceptibility to active disease.

Indexed as

AdultAgedAntibodies, NeutralizingAntigens, BacterialBacterial ProteinsDiabetes Mellitus, Type 2Disease SusceptibilityFemaleHumansInterleukin-10Latent TuberculosisLymphocyte ActivationMaleMiddle AgedTh17 CellsTh1 CellsAntibodies, NeutralizingAntigens, BacterialBacterial ProteinsCFP-10 protein, Mycobacterium bovisInterleukin-10Transforming Growth Factor betaDiabetes ⋅ IL-10 ⋅ Tuberculosis ⋅ Th cells ⋅ TGF-β

Identifiers

PMID26518995
PMCPMC6340057
OpenAlexW1936533610

What OpenQuestion holds

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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.