Evidence map›Paper›PMID 25959254›Full record

ArticleCytokine2015

Impaired toll-like receptor signalling in peripheral B cells from newly diagnosed type-2 diabetic subjects.

Haridoss Madhumitha, Viswanathan Mohan, Nathella P Kumar, Rajendra Pradeepa, Subash Babu, Vivekanandhan Aravindhan

Open access · greenAbstract read
In one paragraph

Article in Cytokine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Trial
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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 4 institutions in 1 country.

Haridoss MadhumithaAU-KBC Research Centre, MIT Campus of Anna University, Chennai 600 044, India.
Viswanathan MohanMadras Diabetes Research Foundation & Dr. Mohan's Diabetes Specialties Centre, WHO Collaborating Centre for Non-Communicable Diseases Prevention and Control, International Diabetes Federation (IDF) Centre for Education, Chennai, India.
Nathella P KumarNational Institutes of Health-International Centre for Excellence in Research, National Institute for Research in Tuberculosis, Chennai, India.
Rajendra PradeepaMadras Diabetes Research Foundation & Dr. Mohan's Diabetes Specialties Centre, WHO Collaborating Centre for Non-Communicable Diseases Prevention and Control, International Diabetes Federation (IDF) Centre for Education, Chennai, India.
Subash BabuNational Institutes of Health-International Centre for Excellence in Research, National Institute for Research in Tuberculosis, Chennai, India.
Vivekanandhan AravindhanAU-KBC Research Centre, MIT Campus of Anna University, Chennai 600 044, India; Dept of Genetics, Dr ALM PG IBMS, University of Madras, Taramani, Chennai, India. Electronic address: cvaravindhan@gmail.com.
Madras Diabetes Research Foundation · INNational Institute of Research in Tuberculosis · INAnna University, Chennai · INUniversity of Madras · 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

Toll-like receptors (TLRs) under diabetic conditions trigger inflammation and impair immunity. In the present study, we looked at the expression of TLRs (2 and 4) and their adaptors in Normal Glucose Tolerant (NGT), Newly Diagnosed Type-2 Diabetic (NDD) and Known Type-2 Diabetic (KDM) subjects. We also estimated TLR induced cytokine secretion, cellular activation and apoptosis. Surface expression of TLR2 and 4 was significantly reduced in the B cells of the NDD subjects and was associated with decreased cellular activation and cytokine secretion (TNF-α and IL-6). This impairment was not due to B cell deficiency or apoptosis or immunosuppressive cytokine (IL-10 and TGF-β) secretion. However, the upregulation of immunomodulatory enzymes (Arg-1, HO-1 and IDO) could probably account for the reduced TLR expression. The defective TLR signalling was largely ameliorated in the KDM group which might be due to the use the anti-diabetic drugs which have anti-inflammatory effect.

Indexed as

AdultAntigens, CDAntigens, Differentiation, T-LymphocyteApoptosisB-LymphocytesCD69 AntigensCells, CulturedDiabetes MellitusFemaleHumansIndoleamine-Pyrrole 2,3,-DioxygenaseInterleukin-10Interleukin-6Lectins, C-TypeMaleMiddle AgedAntigens, CDAntigens, Differentiation, T-LymphocyteCD69 AntigensIDO1 protein, humanIL10 protein, humanIndoleamine-Pyrrole 2,3,-DioxygenaseInterleukin-10Interleukin-6Lectins, C-TypeTNF protein, humanToll-Like Receptor 2Toll-Like Receptor 4Transforming Growth Factor betaTumor Necrosis Factor-alphaCD69IL-6TLR2TLR4TNF-α

Identifiers

PMID25959254
PMCPMC6367209
OpenAlexW266930304

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.