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Eicosapentaenoic acid induces an anti-inflammatory transcriptomic landscape in T cells implicating a pathway independent of triglyceride lowering in cardiovascular risk reduction [RNA-seq]

GSE254695 Homo sapiens (human) RNA-seq (gene expression) 32 samples Submitted 2025/04/30 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 32 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
32 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
EPA Induces an Anti-Inflammatory Transcriptome in T Cells, Implicating a Triglyceride-Independent Pathway in Cardiovascular Risk ReductionJACC. Basic to translational science · 2025
Summary (written by the submitters)
A twice-daily dose of highly purified eicosapentaenoic acid (EPA) reduces the risk of atherosclerotic cardiovascular disease among patients with high triglycerides and either known cardiovascular disease or those at high risk for developing it. However, the process by which EPA exerts its beneficial effects remains ill understood. Here, we show that EPA can induce an anti-inflammatory transcriptional profile in non-activated CD4+ T cells.
Read the full summary ↓
We find that EPA exposed CD4+ T cells downregulate immune response related genes, such as HLA-DRA, CD69, and IL2RA, while upregulating genes involved in oxidative stress prevention, such as NQO1. Furthermore, transcription footprint analysis reveals downregulation of GATA3 and PU.1, key transcription factors in TH2 and TH9 differentiation, and upregulation of REV-ERB, an antagonist of TH17 differentiation. Additionally, we examine T cell responses to two other fatty acids of varying degrees of saturation, namely oleic and palmitic acid, and find EPA has a distinct effect on CD4+ T cells transcriptomic landscape as compared to control. Thus, our study shows that EPA can already induce beneficial transcriptomic profiles in CD4+ T cells prior to activation, a process that may contribute to the unexpectedly strong beneficial effects of EPA on atherosclerotic cardiovascular disease observed in clinical trials.
Published in
EPA Induces an Anti-Inflammatory Transcriptome in T Cells, Implicating a Triglyceride-Independent Pathway in Cardiovascular Risk Reduction
Reilly NA, Dekkers KF, Molenaar J et al. · JACC. Basic to translational science 2025 · PMID 40139879 · doi:10.1016/j.jacbts.2024.09.002
This dataset
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.

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 GSE254695_RAW.tar (it can run to tens of gigabytes).

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.

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 PRJNA1071538 and SRA study SRP487089. Searching any of these in the dataset finder brings you back here.

Samples in this study

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