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Dysbiosis-induced expansion of AXL-positive inflammatory type 3 dendritic cells triggers pre-clinical autoimmunity

GSE297493 Mus musculus (mouse) RNA-seq (gene expression) 14 samples Submitted 2026/06/11 Platform GPL30172
At a glance

RNA-seq (gene expression) · mouse · 14 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
14 samples: 5 conditions, mostly in triplicateGroups 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)
Conventional dendritic cells (cDC) are key sentinels at epithelial barriers, regulating immunity to microbial pathogens and commensals while preserving tissue integrity. NOTCH2 deficiency in CD11c-expressing cells (Notch2cKO) disrupts type 2a DC (cDC2a) development, impairs intestinal TH17 immunity, and increases susceptibility to enteropathogenic bacteria.
Read the full summary ↓
This lead to persistent dysbiosis within our Notch2cKO colony, characterized by low-grade inflammation and systemic autoimmune features, including elevated autoantibody titers and renal immune-complex deposition. Dysbiosis preceded expansion of highly inflammatory AXL-expressing type 3 DC (AXL+inf-DC3), promoting chronic inflammation and tertiary lymphoid structures driving adaptive immune responses. Notably, dysbiosis was defined by three dominant pathobionts and was transferable to WT mice, recapitulating the autoimmune features observed in Notch2cKO mice. Collectively, these findings identify a microbiota–DC axis linking intestinal pathobionts to systemic autoimmunity, establishing inflammatory DC3 as the cellular bridge between dysbiosis, chronic inflammation and autoimmune pathogenesis.
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 GSE297493_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 PRJNA1265080 and SRA study SRP586251. Searching any of these in the dataset finder brings you back here.

Study design
5 conditions, mostly in triplicate
Splenic_cDC2a_Notch2FL ×3 Splenic_DC3_Notch2FL ×3 Splenic_cDC1_Notch2FL ×3 Splenic_cDC1_Notch2cKO ×3 Splenic_DC3_Notch2cKO ×2

Supports a between-group comparison across 14 samples.

How we read this: 5 replicated groups read from 14 sample titles; they account for 14 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.