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The chromatin assembly factor CHAF1b functions as an epigenetic amplifier of RORγt to promote Th17 pathogenicity and autoimmunity

GSE326921 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 13 samples Submitted 2026/04/08 Platform GPL34290
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 13 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
13 samples: 4 × Wild-type vs 3 × Wild-type, vs 3 × KO, vs 2 × KOGroups 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)
Th17 cells are double-edged regulators of mucosal defense and autoimmune inflammation, yet the chromatin mechanisms distinguishing their pathogenic state remain elusive. Here, we identify CHAF1b, a core subunit of the chromatin assembly factor CAF-1 complex, as an essential epigenetic amplifier of RORgt-driven transcription in Th17 cells.
Read the full summary ↓
CHAF1b expression is selectively induced during Th17 differentiation and elevated in inflamed tissues from mice with experimental autoimmune encephalomyelitis (EAE) and colitis. Th17-specific deletion of Chaf1b markedly reduces IL-17A/F expression, alleviates neuroinflammation and colonic pathology, and reprograms the Th17 effector transcriptome without affecting lineage commitment. Mechanistically, CHAF1b physically associates with RORgt and co-occupies enhancer regions at the Il17a–Il17f locus, promoting chromatin accessibility and enhancer activation. Multi-omics analyses reveal that CHAF1b reinforces RORgt-driven enhancer–promoter interactions and maintains a proinflammatory Th17 epigenome. In human Th17 cells, CHAF1b similarly governs IL-17 production, and its expression declines in patients with inflammatory bowel disease following effective therapy. Collectively, these findings uncover CHAF1b as a chromatin-anchored signal amplifier that couples RORgt activity to autoimmune inflammation, highlighting its potential as a therapeutic target for Th17-mediated disorders.
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 GSE326921_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 PRJNA1447944 and SRA study SRP689119. Searching any of these in the dataset finder brings you back here.

Study design
4 × Wild-type vs 3 × Wild-type, vs 3 × KO, vs 2 × KO

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 13 sample titles; they account for 12 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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