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Transcriptionally and phenotypically dysfunctional neutrophils have a suppressive role in macrophage activation syndrome

GSE299930 Mus musculus (mouse) Single-cell RNA-seq 3 samples Submitted 2025/07/15 Platform GPL24247

At a glance

Single-cell RNA-seq · mouse · 3 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: Mus musculus (mouse)
Samples: 3 samples
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)

Macrophage activation syndrome (MAS) is a life-threatening cytokine storm syndrome that complicates rheumatic diseases including systemic juvenile idiopathic arthritis (SJIA). Though neutrophil expansion and activation are key features of SJIA, MAS is associated with neutropenia. As the functional contribution of neutrophils to MAS is largely unexplored, we aimed to define neutrophil dynamics in the TLR9-induced MAS mouse model.

Read the full summary ↓

Mice with TLR9-MAS showed a transient increase in immature neutrophils during MAS and persistent decrease of mature neutrophils through resolution, even after other MAS features were normalized. Single-cell RNA sequencing confirmed increased proportions of both interferon-stimulated gene-high and immature neutrophils during MAS. We also detected an enhanced interferon signature with upregulation of CD274 (PD-L1), suggesting immunosuppressive roles but distinct form myeloid-derived suppressor cells (MDSC). Furthermore, most of the interferon signature normalized at resolution, but prolonged suppression of IL-1 related genes persisted. Neutrophils from both acute and resolution phases of MAS showed in vitro suppression of pro-inflammatory responses upon LPS stimulation. Notably, antibody mediated neutrophil depletion exaggerated clinical, laboratory, and immunologic features of MAS. Overall, neutrophils in MAS show dynamic changes in subpopulations, including transcriptional and phenotypic dysfunction. These findings suggest that mature neutrophils may play anti-inflammatory roles in MAS and highlights an underappreciated role for neutrophil functions in the pathogenesis of cytokine storm syndromes.

This dataset

Open GSE299930 in finder → Find more mouse 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 GSE299930_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 PRJNA1277345 and SRA study SRP592345. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Samples in this study

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+ 3 more — browse all 3 samples with per-sample file links →

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