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Targeting cathepsin B alleviates activation of IL-17A-netrophils axis to suppress atopic dermatitis

GSE314668 Mus musculus (mouse) RNA-seq (gene expression) 12 samples Submitted 2025/12/26 Platform GPL24247
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: 4 × Blank vs 4 × Model vs 4 × IsoLGroups 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)
Atopic dermatitis (AD) is a common chronic relapsing inflammatory skin disease lacking therapeutic drugs that address its complex, heterogeneous pathogenesis. By clinical data analysis and AD model verification, our study demonstrated that lysosomal destabilization and the subsequent cytoplasmic release of cathepsins was a critical pathway that amplifies the Interleukin-17A (IL-17A) inflammatory response and promotes AD progression.
Read the full summary ↓
We revealed that Isoliensinine (IsoL) is a novel therapeutic agent that can target cathepsin B (CTSB) to delay the progression of AD, rather than alleviate symptoms of inflammation. Mechanistically, IsoL significantly suppressed AD and inhibited inflammation, specifically downregulating IL-17A signaling by suppressing dendritic cell mediated Type 17 T-helper cell (Th17) differentiation, thus suppressing neutrophil infiltration. Rescue experiments confirmed that IsoL’s anti-inflammatory and AD-suppressing effects were dependent on its inhibition of CTSB-IL-17A-neutrophil axis. These findings highlighted CTSB as a crucial drug target in AD and present IsoL as a promising novel candidate for AD treatment.
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 GSE314668_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 PRJNA1392434 and SRA study SRP657243. Searching any of these in the dataset finder brings you back here.

Study design
4 × Blank vs 4 × Model vs 4 × IsoL

Supports a between-group comparison across 12 samples.

How we read this: 3 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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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.