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Fibroblast-derived alarmin promotes oral wound healing by activating Tregs that relay pro_x0002_angiogenic and anti-inflammatory

GSE292645 Mus musculus (mouse) Single-cell RNA-seq 2 samples Submitted 2026/01/08 Platform GPL24247
At a glance

Single-cell RNA-seq · mouse · 2 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
2 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)
Fibroblasts are abundant structural cells that produce extracellular matrix components and are essential for tissue repair following an injury. Emerging evidence highlights a crucial immunomodulatory role of fibroblasts in health and disease, which is incompletely explored in the wound healing field. Here, we used an oral wound healing model that heals exceptionally fast with minimal scarring and investigated if select fibroblasts are endowed with immune-regulatory functions that can have an impact on optimal healing outcomes.
Read the full summary ↓
We identified PI16+ oral reticular fibroblasts to be highly enriched in interleukin-33 (IL33), an alarmin cytokine that is rapidly released during the early stages of wound healing. Using mice with lineage-specific, inducible deletion of IL33, we found that baseline expression of IL33 from fibroblasts but not keratinocytes was necessary for proper wound healing in oral mucosa. Singe cell RNA-sequencing (scRNA-seq)analysis revealed that regulatory T cells (Tregs) respond to IL33 and upregulate the expression of a pro-inflammatory cytokine MIF and an anti-inflammatory cytokine TGFB1, which was validated in vivo. Mechanistically, MIF promotes recruitment of angiogenic monocytes to facilitate blood vessel formation in healing wounds, whereas TGFB1 supports an early transition of macrophages to a pro-resolving phenotype. Importantly, we show that human oral mucosa, but not skin, harbors IL33+ PI16+ reticular fibroblasts in deeper aspects of the connective tissue and that Tregs express MIF and TGFB1 in regenerating oral mucosa. Together, our study unveils an essential role of IL33+ oral reticular fibroblasts for the modulation of acute inflammation by engaging Tregs that promote angiogenesis and resolution of inflammation in wound healing.
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 GSE292645_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: 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 PRJNA1238380. Searching any of these in the dataset finder brings you back here.

Samples in this study

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