GEO series

Th2-primed innate immune amplification defines a distinct atopic dermatitis endotype

GSE330551 Homo sapiens (human) RNA-seq (gene expression) 174 samples Submitted 2026/05/13 Platform GPL18573

At a glance

RNA-seq (gene expression) · human · 174 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: Homo sapiens (human)
Samples: 174 samples: 174 samples, each with a distinct title — no replicated groupsGroups 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 clinically heterogeneous, but reproducible molecular endotypes remain incompletely defined. By integrating >1,300 lesional and non-lesional skin transcriptomes from 30 studies, we identified two robust AD endotypes that share a conserved lesional core program of barrier disruption and type 2 activation. In contrast to endotype 1 (62%), endotype 2 (38%) was distinguished by a compact 108-gene innate-inflammatory signature (including IL1B and IL6), increased myeloid infiltration, and Staphylococcus aureus-associated dysbiosis.

Read the full summary ↓

Endotype assignment was stable across longitudinal datasets, with only limited, non-systematic switching upon systemic treatment. Analysis of trial and observational data provided preliminary evidence for lower clinical response and higher residual molecular activity under dupilumab in endotype 2 compared to endotype 1. Interaction modeling of Th2 and innate module activity revealed a Th2-amplified innate state that predicts endotype 2, paralleling functional experiments in which IL-1b/IL-6 synergize with Th2 cytokines to exacerbate keratinocyte inflammation and to impair keratinocyte differentiation. Our findings offer new insights into the biological diversity of AD and establish a robust foundation for mechanistic stratification, with implications for therapeutic strategies.

This dataset

Open GSE330551 in finder → Find more human RNA-seq 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 GSE330551_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: 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 PRJNA1464594 and SRA study SRP699325. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

174 samples, each with a distinct title — no replicated groups

Supports a case/control comparison: 120 samples read as cases, 54 as controls.

How we read this: Read from 174 sample titles: 174 distinct titles with little repetition. 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

GSM9728590 Patient 20, Visit 3/BL, Biopsy Gene, Non Lesion
GSM9728591 Patient 1, Visit 12/ET, Biopsy Hist, Lesion
GSM9728592 Patient 41, Visit 12/ET, Biopsy Gene, Lesion
GSM9728593 Patient 14, Visit 3/BL, Biopsy Gene, Non Lesion
GSM9728594 Patient 17, Visit 3/BL, Biopsy Gene, Lesion
GSM9728595 Patient 15, Visit 5, Biopsy Gene, Lesion
GSM9728596 Patient 34, Visit 3/BL, Biopsy Gene, Lesion
GSM9728597 Patient 10, Visit 5, Biopsy Gene, Lesion
GSM9728598 Patient 24, Visit 12/ET, Biopsy Gene, Lesion
GSM9728599 Patient 23, Visit 12/ET, Biopsy Gene, Lesion
GSM9728600 Patient 45, Visit 3/BL, Biopsy Gene, Lesion
GSM9728601 Patient 3, Visit 12/ET, Biopsy Hist, Lesion
GSM9728602 Patient 2, Visit 5, Biopsy Hist, Lesion
GSM9728603 Patient 40, Visit 3/BL, Biopsy Gene, Lesion
GSM9728604 Patient 25, Visit 12/ET, Biopsy Gene, Lesion
GSM9728605 Patient 31, Visit 3/BL, Biopsy Gene, Lesion
GSM9728606 Patient 22, Visit 3/BL, Biopsy Gene, Lesion
GSM9728607 Patient 42, Visit 3/BL, Biopsy Gene, Lesion
GSM9728608 Patient 6, Visit 5, Biopsy Gene, Lesion
GSM9728609 Patient 21, Visit 3/BL, Biopsy Gene, Non Lesion
GSM9728610 Patient 43, Visit 5, Biopsy Gene, Lesion
GSM9728611 Patient 15, Visit 3/BL, Biopsy Gene, Non Lesion
GSM9728612 Patient 5, Visit 12/ET, Biopsy Hist, Lesion
GSM9728613 Patient 26, Visit 5, Biopsy Gene, Lesion
GSM9728614 Patient 12, Visit 12/ET, Biopsy Gene, Lesion
GSM9728615 Patient 2, Visit 12/ET, Biopsy Hist, Lesion
GSM9728616 Patient 36, Visit 3/BL, Biopsy Gene, Lesion
GSM9728617 Patient 44, Visit 12/ET, Biopsy Gene, Lesion
GSM9728618 Patient 43, Visit 3/BL, Biopsy Gene, Lesion
GSM9728619 Patient 5, Visit 3/BL, Biopsy Hist, Non Lesion
GSM9728620 Patient 15, Visit 12/ET, Biopsy Gene, Lesion
GSM9728621 Patient 21, Visit 12/ET, Biopsy Gene, Lesion
GSM9728622 Patient 33, Visit 12/ET, Biopsy Gene, Lesion
GSM9728623 Patient 6, Visit 3/BL, Biopsy Hist, Non Lesion
GSM9728624 Patient 25, Visit 3/BL, Biopsy Gene, Lesion
GSM9728625 Patient 14, Visit 5, Biopsy Gene, Lesion
GSM9728626 Patient 4, Visit 3/BL, Biopsy Hist, Non Lesion
GSM9728627 Patient 37, Visit 5, Biopsy Gene, Lesion
GSM9728628 Patient 27, Visit 5, Biopsy Gene, Lesion
GSM9728629 Patient 46, Visit 5, Biopsy Gene, Lesion

+ 134 more — browse all 174 samples with per-sample file links →

Datasets on a similar topic

GSE292848 Distinct Roles of IL-4, IL-13, and IL-22 in Human Skin Barrier Dysfunction and Atopic Dermatitis 25 samples shares dermatitis, distinct, atopic
GSE328048 Single-cell transcriptome reveals keratinocyte subclusters that contribute to altered differentiation and inflammatory responses in atopic dermatitis 116 samples shares dermatitis, atopic
GSE232127 Inflammatory signature of atopic dermatitis from tissue and systemic levels 75 samples shares dermatitis, atopic
GSE316337 Multi-omics profiling reveals microbiota, metabolite, lipid, and immunological heterogeneity underlying distinct pathophysiological mechanisms of age-related endotypes in type 1 diabetes 54 samples shares distinct, endotype
GSE309967 Immunometabolic Endotypes Define Distinct Clinical Trajectories in Type 2 Diabetes 48 samples shares distinct, endotype
GSE309941 Immunometabolic Endotypes Define Distinct Clinical Trajectories in Type 2 Diabetes [bulk RNA-seq] 42 samples shares distinct, endotype
GSE326320 Integrative transcriptomic, network, and genomic analysis of peripheral blood mononuclear cells identifies candidate gene drivers of dupilumab clinical response in atopic dermatitis patients 36 samples shares dermatitis, atopic
GSE183953 Comparing PBMCs from patients with atopic dermatitis pre- and post-treatment with dupilumab 16 samples shares dermatitis, atopic

Search all human RNA-seq datasets in GEO →

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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.