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The Transcription Factor IRF8 drives tumor-specific exhaustion in CD8 T cells

GSE333230 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2026/06/05 Platform GPL34475
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 12 samples

What it is
ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism
Mus musculus (mouse)
Samples
12 samples: 10 distinct titles, 1 of them repeatedGroups 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.
Paper
The transcription factor IRF8 drives tumor-specific exhaustion in CD8+ T cellsThe Journal of experimental medicine · 2026
Summary (written by the submitters)
T-cell exhaustion is a hallmark of chronic infection and cancer and constitutes a major barrier for successful immunotherapies. In this study, we establish the central role of IRF8 as a transcription factor regulating tumor-induced T cell exhaustion. IRF8 is highly expressed in CD8 T cells in tumors but not during chronic infection, where the Irf8 locus is less accessible.
Read the full summary ↓
Its expression depends on TCR stimulation but is altered in the presence of type I IFN. Overexpression of IRF8 strongly enforced T cell dysfunction while IRF8 knock-out in tumor specific CD8 T cells reduced TOX expression and ameliorated effector function by increasing IFNγ, GrzB and TNF production, resulting in a better tumor control. By comparing IRF8 to IRF2 and IRF4, we showed that the IRF family display some redundancy in the regulation of T cell exhaustion converging on TOX-dependent programs. Altogether, we established a new role for IRF8 as a tumor specific regulator of T cell function.
Published in
The transcription factor IRF8 drives tumor-specific exhaustion in CD8+ T cells
Ongaro M, Thouenon R, Crespo I et al. · The Journal of experimental medicine 2026 · PMID 42329236 · doi:10.1084/jem.20252115
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 GSE333230_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1470529 and SRA study SRP703655. Searching any of these in the dataset finder brings you back here.

Study design
10 distinct titles, 1 of them repeated
IRF ×3

How we read this: Read from 12 sample titles: 10 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
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