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STING agonists drive recruitment and intrinsic type I interferon responses in monocytic lineage cells for optimal anti-tumor immunity

GSE297709 Mus musculus (mouse) Single-cell RNA-seq 18 samples Submitted 2025/05/20 Platform GPL24247
At a glance

Single-cell RNA-seq · mouse · 18 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
18 samples: 4 × Citeseq, lymph node day 1, ADT, L vs 4 × Citeseq, lymph node day 1, HTO, L vs 4 × Citeseq, tumor day 2, ADT, L vs 4 × Citeseq, tumor day 2, HTO, LGroups 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
STING agonists drive recruitment and intrinsic type I interferon responses in monocytic lineage cells for optimal anti-tumor immunityJournal of immunology (Baltimore, Md. : 1950) · 2025
Summary (written by the submitters)
The cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway, a sensor of cytosolic DNA, orchestrates the production of proinflammatory cytokines, chemokines, and type I interferons (IFN-Is), thereby contributing to spontaneous tumor surveillance. Intratumoral delivery of synthetic STING agonists induces IFN-I-dependent tumor regression in preclinical cancer models and is being tested clinically.
Read the full summary ↓
In this study, we investigate the role of monocytic lineage cells (MCs) in response to STING agonist induced IFN-I signaling. We show that CCR2-deficient mice, lacking inflammatory MCs in the periphery, or Lyz2-Cre-IFNAR1fl/fl mice in which IFN-I signaling in monocytes is reduced, exhibit impaired responses to STING agonist therapy of MC38 and/or B16F10 tumors. STING agonist treatment induced CCR5-dependent migration of MCs carrying tumor antigen from the tumor to the lymph nodes. Single-cell RNA sequencing of CD45+ cells from lymph nodes and tumors of mice in which half the hematopoietic cells lack the IFNAR1 (interferon alpha/beta receptor 1) revealed that STING agonist therapy induces intrinsic IFNAR1-dependent acquisition of an inflammatory monocytic cell phenotype distinct from inflammatory classical dendritic cells (cDC) and a reduction in macrophages with a protumor TGFβ/angiogenesis transcriptome. Interleukin (IL)-18-IL-18R1 interaction was the top predicted interaction between monocytic lineage cells and CD8+ T cells or natural killer cells. Blocking IL-18 reduced IFN-γ production by CD8 T cells in lymph nodes and decreased the therapeutic efficacy of STING agonist treatment in Ccr2+/+ but not in Ccr2-/- mice. These findings support a pivotal role for IL-18 producing inflammatory monocytic lineage cells in CD8+ T cell control of melanoma following STING agonist treatment.
Published in
STING agonists drive recruitment and intrinsic type I interferon responses in monocytic lineage cells for optimal anti-tumor immunity
Girard M, Yu T, Batista NV et al. · Journal of immunology (Baltimore, Md. : 1950) 2025 · PMID 40633091 · doi:10.1093/jimmun/vkaf131
This dataset
Open GSE297709 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 GSE297709_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 PRJNA1265750 and SRA study SRP586725. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40633091) ↗
Study design
4 × Citeseq, lymph node day 1, ADT, L vs 4 × Citeseq, lymph node day 1, HTO, L vs 4 × Citeseq, tumor day 2, ADT, L vs 4 × Citeseq, tumor day 2, HTO, L

Supports a between-group comparison across 16 samples.

How we read this: 4 replicated groups read from 18 sample titles; they account for 16 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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