Evidence map›Paper›PMID 24693923›Full record

ArticleJournal of diabetes and metabolic disorders2014

TNF-α and IFN-γ gene variation and genetic susceptibility to type 1 diabetes and its microangiopathic complications.

Javad Tavakkoly Bazzaz, Mahsa M Amoli, Zahra Taheri, Bagher Larijani, Vera Pravica, Ian V Hutchinson

Open access · hybridAbstract read
In one paragraph

Article in Journal of diabetes and metabolic disorders, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Trial
  2. Defective efferocytosis in diabetes: molecular mechanisms and emerging therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
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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 2 institutions in 2 countries.

Javad Tavakkoly BazzazDepartment of Medical Genetics, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Mahsa M AmoliEndocrinology and Metabolism Research Centre, Tehran University of Medical Sciences, Tehran, Iran.
Zahra TaheriEndocrinology and Metabolism Research Centre, Tehran University of Medical Sciences, Tehran, Iran.
Bagher LarijaniEndocrinology and Metabolism Research Centre, Tehran University of Medical Sciences, Tehran, Iran.
Vera PravicaSchool of Pharmacy, University of Southern California (USC), Los Angeles, USA.
Ian V HutchinsonSchool of Pharmacy, University of Southern California (USC), Los Angeles, USA.
Tehran University of Medical Sciences · IRUniversity of Southern California · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTNF-α has accelerating role in development of type 1 diabetes. Although an immunosupressor function and leading protecting role in T1DM also has been claimed for this pro-inflammatory cytokine. Over-expression of pro-inflammatory and type 1 cytokines (Th1, like IFN-γ) drive insulitis toward the destructive form that leads to type 1 diabetes (T1DM). Among type 1 cytokines only IFN-γ has been detectable in the islet β cells. In deletion studies IFN-γ was also the only Th1 cytokine for which its ablation or blockade caused delayed or decreased incidence of T1DM.

methodsFunctional polymorphisms of TNF-α at position -308*G/A and at position +874*T/A of IFN-γ gene were employed as markers and the comparative distribution of derived genotypes/alleles were assessed in 248 British Caucasian T1DM patients and 118 healthy controls.

resultsThere was no significant association between IFN-γ gene polymorphism and T1DM or the diabetic complication triad. There was a marginal association between TNF-α -308*G/A polymorphism in nephropaths (vs healthy controls) (p = 0.06), which its insignificancy may be due to survivor factor. No significant association was evident between the genotype/allele of the applied marker and T1DM or diabetic complication triad.

conclusionOur results are in contrast with previous reports suggesting that these polymorphisms are not related to T1DM. This study also underlines the importance of replication of association studies to confirm the previous interpretation.

Identifiers

PMID24693923
PMCPMC4000155
OpenAlexW2132355417

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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.