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Citraconate preserves T cell stemness and antitumor immunity

GSE326246 Mus musculus (mouse) RNA-seq (gene expression) 9 samples Submitted 2026/04/06 Platform GPL19057
At a glance

RNA-seq (gene expression) · mouse · 9 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
Mus musculus (mouse)
Samples
9 samples: 3 × CTRL vs 3 × OVA vs 3 × OVA/CitraGroups 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; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Summary (written by the submitters)
Metabolic perturbations within the tumor microenvironment profoundly compromise the stem-like properties and functionality of CD8+ T cells. Elucidating the metabolic circuitry that maintains T cell stemness is therefore essential for rejuvenating tumor-infiltrating lymphocytes and enhancing immunotherapeutic efficacy. Here, we identify citraconate, an itaconate isomer, as a critical metabolite markedly depleted in CD8+ T cells under chronic antigen stimulation or hypoxia.
Read the full summary ↓
Citraconate supplementation preserves stem-like properties, mitigates ferroptosis, and potentiates T cell-mediated antitumor efficacy. Mechanistically, citraconate sustains intracellular cAMP pool by suppressing phosphodiesterase (PDE1A/C) expression and maintaining mitochondrial integrity, thereby activating protein kinase A (PKA) signaling. This activation represses arachidonate-5-lipoxygenase (ALOX5) transcription, reducing arachidonic acid peroxidation. Clinically, reduced ALOX5 or PDE1A expression correlates with decreased T cell exhaustion and enhanced responses to immune checkpoint blockade (ICB) therapy. Our findings reveal the citraconate-mediated PDE1-cAMP-ALOX5 axis as a promising therapeutic target for potentiating cancer immunotherapy.
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 GSE326246_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 PRJNA1444995 and SRA study SRP687608. Searching any of these in the dataset finder brings you back here.

Study design
3 × CTRL vs 3 × OVA vs 3 × OVA/Citra

Supports a between-group comparison across 9 samples.

How we read this: 3 replicated groups read from 9 sample titles; they account for 9 of them. 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
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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.