GEO series

Dermatomyositis is characterized by JAK1-mediated monocyte-driven vasculopathy and inflammation

GSE303609 Homo sapiens (human) Single-cell RNA-seq 34 samples Submitted 2025/12/24 Platform GPL24676

At a glance

Single-cell RNA-seq · human · 34 samples

What it is: Single-cell RNA-seqGene activity measured in thousands of individual cells, so cell types can be told apart. Read from the summary: GEO's own type field only says 'expression profiling by sequencing', so confirm it in the paper.
Organism: Homo sapiens (human)
Samples: 34 samples: 27 distinct titles, 1 of them repeatedGroups 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: Dermatomyositis is characterized by JAK1-mediated monocyte-driven vasculopathy and inflammationScience translational medicine · 2025

Summary (written by the submitters)

Dermatomyositis (DM) is a rare yet devastating autoimmune disease characterized by inflammatory and vasculopathic changes in skin and muscle. DM and systemic lupus erythematosus (lupus) skin lesions have overlapping clinical and histopathological features, yet disparate responses to available therapeutics. DM skin disease is often relapsing and recalcitrant.

Read the full summary ↓

To investigate DM immunopathogenesis, non-lesional skin, lesional skin, and circulating immune cells from DM patients were analyzed using single-cell RNA-sequencing. Samples were analyzed in parallel with lesional and non-lesional lupus skin, healthy control skin, and peripheral blood. We demonstrate a pervasive type I interferon (IFN) signature in DM stroma that persists in culture and is distinguished from lupus by upregulation of VEGF and IL-18 signaling in DM keratinocytes. Furthermore, endothelial cells (ECs) in lesional DM exhibit decreased proliferation that was not observed in lupus. Using cell communication networks, we identified a population of DM-specific monocytes interacting with non-proliferating DM ECs. Co-culture of monocytes from DM patients with ECs resulted in increased EC apoptosis inhibited by JAK1 blockade. JAK1 inhibition also resulted in reversal of DM-stromal and inflammatory signatures. Together, our data provide a comprehensive cross-disease characterization of lesional and non-lesional skin of DM compared to lupus and implicate monocyte-mediated EC dysfunction in DM vasculopathy and support JAK inhibition for refractory skin disease.

Published in

Dermatomyositis is characterized by JAK1-mediated monocyte-driven vasculopathy and inflammation

Osborne GA, Zhang L, Ma F et al. · Science translational medicine 2025 · PMID 41442501 · doi:10.1126/scitranslmed.aea9007

This dataset

Open GSE303609 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 GSE303609_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: Single-cell studies usually ship their counts as 10x files (matrix.mtx, barcodes.tsv, features.tsv), an .h5 file, or an .rds / .h5ad object that Seurat or Scanpy can open. Look for those among the supplementary files.

Also filed as BioProject PRJNA1295914 and SRA study SRP603524. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41442501) ↗

Study design

27 distinct titles, 1 of them repeated

CTL, Donor A ×8

Supports a case/control comparison: 26 samples read as cases, 8 as controls.

How we read this: Read from 34 sample titles: 27 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

GSM9131361 CTL, Donor AR010
GSM9131362 CTL, Donor AR012
GSM9131363 CTL, Donor AR015
GSM9131364 CTL, Donor AR016
GSM9131365 CTL, Donor AR017
GSM9131366 CTL, Donor AR019
GSM9131367 CTL, Donor AR021
GSM9131368 CTL, Donor AR022
GSM9131369 DM, Donor AB3121, Lesional
GSM9131370 DM, Donor AB3121, Non Lesional
GSM9131371 DM, Donor AB3970, Lesional
GSM9131372 DM, Donor AB3970, Non Lesional
GSM9131373 DM, Donor AB4267, Lesional
GSM9131374 DM, Donor AB4267, Non Lesional
GSM9131375 DM, Donor AB4312, Lesional
GSM9131376 DM, Donor AB4312, Non Lesional
GSM9131377 DM, Donor AB4547, Lesional
GSM9131378 DM, Donor AB4547, Non Lesional
GSM9131379 DM, Donor AB4685, Lesional
GSM9131380 DM, Donor AB4685, Non Lesional
GSM9131383 DM, Donor AB496, Lesional
GSM9131386 DM, Donor AB496, Non Lesional
GSM9131387 DM, Donor MW288, Lesional
GSM9131388 DM, Donor MW288, Non Lesional
GSM9131389 SLE, Donor AB3149, Lesional
GSM9131390 SLE, Donor AB3149, Non Lesional
GSM9131391 SLE, Donor AB4016, Lesional
GSM9131392 SLE, Donor AB4016, Non Lesional
GSM9131393 SLE, Donor AB4022, Lesional
GSM9131394 SLE, Donor AB4022, Non Lesional
GSM9131395 SLE, Donor AB4801, Lesional
GSM9131396 SLE, Donor AB4801, Non Lesional
GSM9131397 SLE, Donor AB4887, Lesional
GSM9131398 SLE, Donor AB4887, Non Lesional

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