Evidence map›Paper›PMID 23148518›Full record

ArticleClinical epigenetics2012

Genome-scale case-control analysis of CD4+ T-cell DNA methylation in juvenile idiopathic arthritis reveals potential targets involved in disease.

Justine A Ellis, Jane E Munro, Raul A Chavez, Lavinia Gordon, Jihoon E Joo, Jonathan D Akikusa, Roger C Allen, Anne-Louise Ponsonby, Jeffrey M Craig, Richard Saffery

Open access · goldAbstract read
In one paragraph

Article in Clinical epigenetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
11.8field-weighted citation impact, top 1% 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

29 citing papers in PubMed, 46 citations in OpenAlex.

  1. Differential transcriptional and epigenetic signatures in CD4Journal of translational autoimmunity · 2026
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  10. Epigenetics and sarcoidosis.European respiratory review : an official journal of the European Respiratory Society · 2021
    Review
  11. Article
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  13. Observational
  14. Immunomics in Pediatric Rheumatic Diseases.Frontiers in medicine · 2019
    Review
  15. Review
  16. Article
  17. Review
  18. Epipolymorphisms associated with the clinical outcome of autoimmune arthritis affect CD4+ T cell activation pathways.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  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

10 authors at 1 institution in 1 country.

Justine A EllisGenes, Environment & Complex Disease, Murdoch Childrens Research Institute, 50 Flemington Rd, Parkville, Vic, Australia. justine.ellis@mcri.edu.au.
Jane E Munro
Raul A Chavez
Lavinia Gordon
Jihoon E Joo
Jonathan D Akikusa
Roger C Allen
Anne-Louise Ponsonby
Jeffrey M Craig
Richard Saffery
Murdoch Children's Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelled

backgroundJuvenile Idiopathic Arthritis (JIA) is a complex autoimmune rheumatic disease of largely unknown cause. Evidence is growing that epigenetic variation, particularly DNA methylation, is associated with autoimmune disease. However, nothing is currently known about the potential role of aberrant DNA methylation in JIA. As a first step to addressing this knowledge gap, we have profiled DNA methylation in purified CD4+ T cells from JIA subjects and controls. Genomic DNA was isolated from peripheral blood CD4+ T cells from 14 oligoarticular and polyarticular JIA cases with active disease, and healthy age- and sex-matched controls. Genome-scale methylation analysis was carried out using the Illumina Infinium HumanMethylation27 BeadChip. Methylation data at >25,000 CpGs was compared in a case-control study design.

resultsMethylation levels were significantly different (FDR adjusted p<0.1) at 145 loci. Removal of four samples exposed to methotrexate had a striking impact on the outcome of the analysis, reducing the number of differentially methylated loci to 11. The methotrexate-naive analysis identified reduced methylation at the gene encoding the pro-inflammatory cytokine IL32, which was subsequently replicated using a second analysis platform and a second set of case-control pairs.

conclusionsOur data suggests that differential T cell DNA methylation may be a feature of JIA, and that reduced methylation at IL32 is associated with this disease. Further work in larger prospective and longitudinal sample collections is required to confirm these findings, assess whether the identified differences are causal or consequential of disease, and further investigate the epigenetic modifying properties of therapeutic regimens.

Identifiers

PMID23148518
PMCPMC3536591
OpenAlexW2118283513

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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.