GEO series

IL-21 Shapes the B Cell Response in a Context-Dependent Manner [CUT&RUN]

GSE280837 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 13 samples Submitted 2025/01/01 Platform GPL24247

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: 2 × B cell, WT, aCD40 + IL-4, IgM, vs 2 × B cell, WT, aCD40 + IL-4, IgG1, vs 2 × B cell, WT, aCD40 + IL-21, IgM, vs 2 × B cell, WT, aCD40 + IL-21, IgG1,Groups 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)

The cytokine interleukin-21 (IL-21) is a pivotal T cell-derived signal crucial for germinal center (GC) responses, but the precise mechanisms by which IL-21 influences B cell function remain elusive. Here, we investigated the B cell-intrinsic role of IL-21 signaling by employing a novel IL-21 receptor (Il21r) conditional knock-out mouse model and ex vivo culture systems and uncovered a surprising duality of IL-21 signaling in B cells.

Read the full summary ↓

While IL-21 stimulation of naïve B cells led to Bim-dependent apoptosis, it promoted robust proliferation of pre-activated B cells, particularly class-switched IgG1+ B cells ex vivo. Consistent with this, B cell-specific deletion of Il21r led to a severe defect in IgG1 responses in vivo following immunization. Intriguingly, Il21r-deleted B cells are significantly impaired in their ability to transition from a pre-GC to a GC state following immunization. Although Il21r-deficiency did not affect the proportion of IgG1+ B cells among GC B cells, it greatly diminished the proportion of IgG1+ B cells among the plasmablast/plasma cell population. Collectively, our data suggest that IL-21 serves as a critical regulator of B cell fates, influencing B cell apoptosis and proliferation in a context-dependent manner.

This dataset

Open GSE280837 in finder → Find more mouse ChIP / ATAC / CUT&Tag 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 GSE280837_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1180890 and SRA study SRP542566. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

2 × B cell, WT, aCD40 + IL-4, IgM, vs 2 × B cell, WT, aCD40 + IL-4, IgG1, vs 2 × B cell, WT, aCD40 + IL-21, IgM, vs 2 × B cell, WT, aCD40 + IL-21, IgG1,

Supports a between-group comparison across 8 samples.

How we read this: 4 replicated groups read from 13 sample titles; they account for 8 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

GSM8606392 B cell, Input
GSM8606393 B cell, WT, aCD40 + IL-4, IgM, rep1 B cell, WT, aCD40 + IL-…
GSM8606394 B cell, WT, aCD40 + IL-4, IgM, rep2 B cell, WT, aCD40 + IL-…
GSM8606395 B cell, WT, aCD40 + IL-4, IgG1, rep1 B cell, WT, aCD40 + IL-…
GSM8606396 B cell, WT, aCD40 + IL-4, IgG1, rep2 B cell, WT, aCD40 + IL-…
GSM8606397 B cell, WT, aCD40 + IL-21, IgM, rep1 B cell, WT, aCD40 + IL-…
GSM8606398 B cell, WT, aCD40 + IL-21, IgM, rep2 B cell, WT, aCD40 + IL-…
GSM8606399 B cell, WT, aCD40 + IL-21, IgG1, rep1 B cell, WT, aCD40 + IL-…
GSM8606400 B cell, WT, aCD40 + IL-21, IgG1, rep2 B cell, WT, aCD40 + IL-…
GSM8606401 B cell, STAT3 KO, aCD40 + IL-4, IgM, rep1
GSM8606402 B cell, STAT3 KO, aCD40 + IL-4, IgG1, rep1
GSM8606403 B cell, STAT3 KO, aCD40 + IL-21, IgM, rep1
GSM8606404 B cell, STAT3 KO, aCD40 + IL-21, IgG1, rep1

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