GEO series
Multi-omics analysis in primary T cells elucidates mechanisms behind disease associated genetic loci [Hi-C]
Summary
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. 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
Download
Direct links to NCBI, no account and no request form: the whole study as GSE282510_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 108 samples.
Also filed as BioProject PRJNA1185164. Searching any of these in the dataset finder brings you back here.
Study design
40 conditions, each sampled once — no replicated groups
Read from the first 40 of 108 sample titles: 40 distinct titles with little repetition. Check it against the sample list below before relying on it.
Samples in this study
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- GSM8644737 NRHV014XCD4, HiC
- GSM8644738 NRHV014XCD8, HiC
- GSM8644739 NRHV056CD8SF, HiC
- GSM8644740 NRHV073_CD4, HiC
- GSM8644741 NRHV073_CD8, HiC
- GSM8644742 NRHV079CD4, HiC
- GSM8644743 NRHV079CD8, HiC
- GSM8644744 NRHV086CD4, HiC
- GSM8644745 NRHV086CD8, HiC
- GSM8644746 NRHV121_CD4, HiC
- GSM8644747 NRHV121_CD8, HiC
- GSM8644748 NRHV151CD4, HiC
- GSM8644749 NRHV168CD4, HiC
- GSM8644750 NRHV168CD8, HiC
- GSM8644751 NRHV171CD4, HiC
- GSM8644752 NRHV171CD8, HiC
- GSM8644753 NRHV238_CD4, HiC
- GSM8644754 NRHV238_CD8, HiC
- GSM8644755 NRHV290CD4, HiC
- GSM8644756 NRHV290CD8, HiC
- GSM8644757 NRHV295CD4, HiC
- GSM8644758 NRHV295CD8, HiC
- GSM8644759 NRHV321_CD4, HiC
- GSM8644760 NRHV321_CD8, HiC
- GSM8644761 NRHV322_CD4, HiC
- GSM8644762 NRHV322_CD8, HiC
- GSM8644763 NRHV324CD4, HiC
- GSM8644764 NRHV324CD8, HiC
- GSM8644765 NRHV325CD4, HiC
- GSM8644766 NRHV325CD8, HiC
- GSM8644767 NRHV326CD4, HiC
- GSM8644768 NRHV326CD8, HiC
- GSM8644769 NRHV332CD4, HiC
- GSM8644770 NRHV332CD8, HiC
- GSM8644771 NRSF055CD8SF, HiC
- GSM8644772 PSA4920_CD4, HiC
- GSM8644773 PSA4920_CD8, HiC
- GSM8644774 PSA4941_CD8, HiC
- GSM8644775 PSA4942_CD4, HiC
- GSM8644776 PSA4942_CD8, HiC
+ 68 more — browse all 108 samples with per-sample file links →
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