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An adaptive cellular source of IL-17A and IL-17F is critical for the induction of experimental autoimmune encephalomyelitis II

GSE324712 Mus musculus (mouse) RNA-seq (gene expression) 12 samples Submitted 2026/07/02 Platform GPL30172
At a glance

RNA-seq (gene expression) · mouse · 12 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
12 samples: 6 × CD4+cxcr6+ vs 6 × CD4+slamf6+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.
Paper
An adaptive cellular source of IL-17A and IL-17F is critical for the induction of experimental autoimmune encephalomyelitisScience immunology · 2026
Summary (written by the submitters)
T helper 17 (TH17) cells have been suggested to play an important role in the pathogenesis of many autoimmune disorders, including multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). However, recent studies suggest that interleukin (IL)-17 may be dispensable for the induction of EAE. Here, we use an adoptive transfer model of EAE to demonstrate that an adaptive cellular source of IL-17 is absolutely required for the induction of EAE disease.
Read the full summary ↓
We further show that B cells can regulate the transfer of EAE disease in this context. Transcriptional profiling of TH17 cells in our model suggest that loss of IL-17A/F in T cells results in a lack of an IL-23 receptor (IL23R)–driven signaling signature. Our data demonstrates the critical importance of an adaptive immune cellular source of IL-17A and IL-17F to mediate EAE, and that IL-17 signaling is required for IL-23-mediated TH17 cell pathogenicity.
Published in
An adaptive cellular source of IL-17A and IL-17F is critical for the induction of experimental autoimmune encephalomyelitis
Ho AW, Huang L, Sandhu S et al. · Science immunology 2026 · PMID 42030372 · doi:10.1126/sciimmunol.aee1481
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 GSE324712_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 PRJNA1436617 and SRA study SRP683254. Searching any of these in the dataset finder brings you back here.

Study design
6 × CD4+cxcr6+ vs 6 × CD4+slamf6+

Supports a between-group comparison across 12 samples.

How we read this: 2 replicated groups read from 12 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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