Evidence map›Paper›PMID 24763540›Full record

ReviewLupus2014

Environmental exposures, epigenetic changes and the risk of lupus.

E C Somers, B C Richardson

Abstract readReview
In one paragraph

Review in Lupus, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 2 pooled it
13.0field-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

59 citing papers in PubMed, 2 syntheses or guidelines pooled it, 115 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Biomolecules & biomedicine · 2025
    Article
  6. Enhancement of CD8Journal of translational autoimmunity · 2025
    Article
  7. Article
  8. Article
  9. Environmental and Genetic Determinants of Ankylosing Spondylitis.International journal of molecular sciences · 2024
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Contribution of Dysregulated DNA Methylation to Autoimmunity.International journal of molecular sciences · 2021
    Review
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

2 authors at 2 institutions in 1 country.

E C Somers1Department of Medicine, University of Michigan, Ann Arbor, USA.
B C Richardson
Ann Arbor VA Medical Center · USUniversity of Michigan–Ann Arbor · US

Funding

Strategic Vision & Impact on Environmental HealthP30ES017885 · NIEHS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Dana Dolinoy · 2011 to 2026
$21.3M
T-CELLS AND THE INDUCTION OF LUPUSR01AR042525 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RICHARDSON, BRUCE C. · 1993 to 2013
$3.8M
Immune dysfunction associated with early life heavy metal exposureK01ES019909 · NIEHS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SOMERS, EMILY CATHERINE · 2011 to 2015
$670k
NIAMS NIH HHS AR42525NIAMS NIH HHS R01 AR042525NIEHS NIH HHS K01 ES019909NIEHS NIH HHS K01ES019909NIEHS NIH HHS P30 ES017885NIEHS NIH HHS P30ES017885
6 · The paper itself

Abstract

A dose-dependent combination of environmental exposures, estrogenic hormones and genetic predisposition is thought to be required for lupus to develop and flare, but how the environment modifies the immune system in genetically predisposed people is unclear. Current evidence indicates that environmental agents that inhibit DNA methylation can convert normal antigen-specific CD4+ T lymphocytes into autoreactive, cytotoxic, pro-inflammatory cells that are sufficient to cause lupus-like autoimmunity in animal models, and that the same changes in DNA methylation characterize CD4+ T cells from patients with active lupus. Environmental agents implicated in inhibiting T-cell DNA methylation include the lupus-inducing drugs procainamide and hydralazine, as well as diet, and agents causing oxidative stress, such as smoking, UV light exposure, and infections, which have been associated with lupus onset or disease activity. Other studies demonstrate that demethylated T cells cause only anti-DNA antibodies in mice lacking a genetic predisposition to lupus, but are sufficient to cause lupus-like autoimmunity in genetically predisposed mice and likely people, and that estrogens augment the disease. Collectively, these studies suggest that environmental agents that inhibit DNA methylation, together with lupus genes and estrogens or endocrine disruptors, combine in a dose-dependent fashion to cause lupus flares.

Indexed as

AnimalsAutoantibodiesDNA MethylationDose-Response Relationship, DrugEndocrine DisruptorsEnvironmental ExposureEnvironmental PollutantsEpigenesis, GeneticGenetic Predisposition to DiseaseHumansLupus Erythematosus, SystemicPrognosisRisk AssessmentRisk FactorsT-LymphocytesAutoantibodiesEndocrine DisruptorsEnvironmental Pollutantsendocrine disruptorsenvironmentepigeneticsgeneticsLupusmercuryoxidative stress

Identifiers

PMID24763540
PMCPMC4000546
OpenAlexW2064968846

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.