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Multi-omics analysis in primary T cells elucidates mechanisms behind disease associated genetic loci [Hi-C]

GSE282510 Homo sapiens (human) Other 108 samples Submitted 2024/12/18 Platform GPL24676
At a glance

human · 108 samples

Organism
Homo sapiens (human)
Samples
108 samples: 108 samples, each with a distinct title — no replicated groupsGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI.
Paper
Multi-omics analysis in primary T cells elucidates mechanisms behind disease-associated genetic lociGenome biology · 2025
Summary (written by the submitters)
Background: Genome wide association studies (GWAS) have uncovered the genetic basis behind many diseases and conditions. However, most of these genetic loci affect regulatory regions, making the interpretation challenging. Chromatin conformation has a fundamental role in gene regulation and is frequently used to associate potential target genes to regulatory regions.
Read the full summary ↓
However, previous studies mostly used small sample sizes and immortalized cell lines instead of primary cells. Results: Here we present the most extensive dataset of chromatin conformation with matching gene expression and chromatin accessibility from primary CD4+ and CD8+ T cells to date, isolated from psoriatic arthritis patients and healthy controls. We generated 108 Hi-C libraries (49 billion reads), 128 RNA-seq libraries and 126 ATAC-seq libraries. These data enhance our understanding of the mechanisms by which GWAS variants impact gene regulation, revealing how genetic variation alters chromatin accessibility and structure in primary cells at an unprecedented scale. We refine the mapping of GWAS loci to implicated regulatory elements, such as CTCF binding sites and other enhancer elements, aiding gene assignment. We uncover BCL2L11 as the probable causal gene within the rheumatoid arthritis (RA) locus rs13396472, despite the GWAS variants’ intronic positioning relative to ACOXL, and we identify mechanisms involving SESN3 dysregulation in the RA locus rs4409785. Conclusions: Given these genes’ significant role in T cell development and maturation, our work deepens our comprehension of autoimmune disease pathogenesis, suggesting potential treatment targets. In addition, our dataset provides a valuable resource for the investigation of immune mediated diseases and gene regulatory mechanisms.
Published in
Multi-omics analysis in primary T cells elucidates mechanisms behind disease-associated genetic loci
Shi C, Zhao D, Butler J et al. · Genome biology 2025 · PMID 39930543 · doi:10.1186/s13059-025-03492-y
This dataset
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Download · which file do I need?

Direct links to NCBI, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓
2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need.

All supplementary files ↗
3 · The original raw files

Whole study · RAW.tar

Everything the authors deposited as one archive (GSE282510_RAW.tar), including the raw array or instrument files. Can be large; the picker in step 2 takes just the samples you need.

Whole study · RAW.tar ↓

Also filed as BioProject PRJNA1185164. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 39930543) ↗
Study design
108 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 108 sample titles: 108 distinct titles with little repetition. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study

+ 68 more — browse all 108 samples with per-sample file links →

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