Evidence map›Paper›PMID 27906046›Full record

ArticleArthritis research & therapy2016

Chromatin landscapes and genetic risk in systemic lupus.

Joyce S Hui-Yuen, Lisha Zhu, Lai Ping Wong, Kaiyu Jiang, Yanmin Chen, Tao Liu, James N Jarvis

Abstract read
In one paragraph

Article in Arthritis research & therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Trial
  2. Aberrant Enhancer Regulation, Phase Separation, and Autoimmune Diseases.Clinical reviews in allergy & immunology · 2025
    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

7 authors.

Joyce S Hui-YuenDivision of Pediatric Rheumatology, Steven and Alexandra Cohen Children's Medical Center, 1991 Marcus Avenue, Suite M100, Lake Success, NY, 11042, USA. jhuiyuen@nshs.edu.
Lisha ZhuDepartment of Biochemistry, University at Buffalo, Buffalo, NY, 14203, USA.
Lai Ping WongDepartment of Pediatrics, University at Buffalo, Buffalo, NY, 14203, USA.
Kaiyu JiangDepartment of Pediatrics, University at Buffalo, Buffalo, NY, 14203, USA.
Yanmin ChenDepartment of Pediatrics, University at Buffalo, Buffalo, NY, 14203, USA.
Tao LiuDepartment of Biochemistry, and Genetics, Genomics, and Bioinformatics Program, University at Buffalo, Buffalo, NY, 14203, USA.
James N JarvisGenetics, Genomics, and Bioinformatics Program, University at Buffalo, Buffalo, NY, 14203, USA.

Funding

Microarray-Based Biomarkers in Juvenile Idiopathic ArthritisR01AR060604 · NIAMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI JARVIS, JAMES N · 2011 to 2015
$2.6M
NIAMS NIH HHS R01 AR060604
6 · The paper itself

Abstract

backgroundSystemic lupus erythematosus (SLE) is a multi-system, complex disease in which the environment interacts with inherited genes to produce broad phenotypes with inter-individual variability. Of 46 single nucleotide polymorphisms (SNPs) shown to confer genetic risk for SLE in recent genome-wide association studies, 30 lie within noncoding regions of the human genome. We therefore sought to identify and describe the functional elements (aside from genes) located within these regions of interest.

methodsWe used chromatin immunoprecipitation followed by sequencing to identify epigenetic marks associated with enhancer function in adult neutrophils to determine whether enhancer-associated histone marks were enriched within the linkage disequilibrium (LD) blocks encompassing the 46 SNPs of interest. We also interrogated available data in Roadmap Epigenomics for CD4

resultsAll three cell types demonstrated enrichment of enhancer-associated histone marks compared with genomic background within LD blocks encoded by SLE-associated SNPs. In addition, within the promoter regions of these LD blocks, all three cell types demonstrated enrichment for transcription factor binding sites above genomic background. In CD19

conclusionsMuch of the genetic risk for SLE lies within or near genomic regions of disease-relevant cells that are enriched for epigenetic marks associated with enhancer function. Elucidating the specific roles of these noncoding elements within these cell-type-specific genomes will be crucial to our understanding of SLE pathogenesis.

Indexed as

B-LymphocytesCD4-Positive T-LymphocytesChromatinChromatin ImmunoprecipitationEnhancer Elements, GeneticEpigenesis, GeneticGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansLinkage DisequilibriumLupus Erythematosus, SystemicPolymorphism, Single NucleotideChromatinEnhancersGeneticsLymphocytesNeutrophilsSystemic lupus erythematosus

Identifiers

PMID27906046
PMCPMC5134118

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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.