GEO series

Autoreactive effector Treg cells with a compromised regulatory program in patients with coronary artery disease

GSE279783 Homo sapiens (human) RNA-seq (gene expression) 144 samples Submitted 2025/05/03 Platform GPL24676

At a glance

RNA-seq (gene expression) · human · 144 samples

What it is: RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism: Homo sapiens (human)
Samples: 144 samples
Data you can get: A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper: Loss of effector T(reg) signature in APOB-reactive CD4(+) T cells in patients with coronary artery diseaseNature cardiovascular research · 2025

Summary (written by the submitters)

Atherosclerosis, a pathological condition underlying cardiovascular diseases, involves chronic inflammation with a strong autoimmune component. Detailed molecular definition of autoreactive CD4+T cells in atherosclerotic patients is critical for understanding their role in disease pathogenesis. Apolipoprotein B (APOB) is a clinically relevant atherosclerosis-related autoantigen.

Read the full summary ↓

Here, we used an activation-induced marker assay to conduct deep transcriptomic analyses of circulating APOB-reactive CD4+T cells from 40 patients with coronary artery disease. We identified autoreactive T cells expressing tissue-homing chemokine receptors and effector Treg signatures, suggesting recirculation of APOB-specific CD4+T cells between blood and atherosclerotic plaques. Treg gene signature and oligoclonality peaked in patients with mild disease, but declined in those with severe atherosclerosis. By contrast, clonal expansion and expression of effector molecules in inflammatory APOB-specific CD4+T cells increased with progressing disease severity. Thus, the autoimmune response in atherosclerosis starts with an atheroprotective regulatory program but switches to an inflammatory phenotype, likely accelerating disease progression.

Published in

Loss of effector T(reg) signature in APOB-reactive CD4(+) T cells in patients with coronary artery disease

Roy P, Bellapu A, Suthahar SSA et al. · Nature cardiovascular research 2025 · PMID 40533521 · doi:10.1038/s44161-025-00671-9

This dataset

Open GSE279783 in finder → Find more human RNA-seq datasets →

Download · which file do I need?

Direct links to NCBI and ENA, 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, or the whole study as GSE279783_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1174673 and SRA study SRP539324. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40533521) ↗

Samples in this study

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+ 144 more — browse all 144 samples with per-sample file links →

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