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Macrophages expressing chimeric cytokine receptors have an inflammatory phenotype and anti-tumoral activity upon IL-10 or TGFβ stimulation

GSE280810 Homo sapiens (human) RNA-seq (gene expression) 30 samples Submitted 2025/10/06 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 30 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)
Topic
Breast cancerThis series is part of our curated briefing on it.
Samples
30 samples: 30 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.
Paper
Macrophages expressing chimeric cytokine receptors have an inflammatory phenotype and antitumoral activity upon IL-10 or TGFβ stimulationJournal for immunotherapy of cancer · 2025
Summary (written by the submitters)
Background Triple-negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer that lacks hormone receptors and HER2 amplification, making it unresponsive to standard hormone or HER2-targeted therapies. Although immune checkpoint inhibitors (ICIs) have shown promise in tumors with high lymphocyte infiltration, their efficacy remains limited in tumors with minimal lymphocyte infiltration.
Read the full summary ↓
To overcome this challenge, we developed a novel approach to reprogram tumor-associated macrophages (TAMs) from an immunosuppressive to an inflammatory phenotype within the tumor microenvironment (TME), aiming to enhance therapeutic outcomes in TNBC. Methods We designed a chimeric cytokine receptor (ChCR) that triggers STAT1 signaling upon stimulation with IL-10 or TGFβ, cytokines prevalent in the TME that typically drive immunosuppression. Human primary macrophages were transduced with a lentiviral vector expressing the ChCR, and changes in their phenotype, secretome, and transcriptome were analyzed following stimulation. The anti-tumoral activity of these reprogrammed macrophages was assessed using co-culture assays with 3D TNBC spheroids. Results ChCR-expressing macrophages showed robust STAT1 activation in response to IL-10 or TGFβ stimulation, resulting in an inflammatory phenotype similar to IFNγ activation, as confirmed by phenotypic markers, and transcriptomic profiling. These ChCR-stimulated macrophages demonstrated significant anti-tumoral effects in 3D TNBC spheroids. Moreover, ChCR stimulation led to the upregulation of CXCL9 and CXCL10, chemokines essential for lymphocyte recruitment, and genes associated with good response to ICIs. Conclusion We successfully engineered a ChCR that reprograms TAMs within an IL-10- and TGFβ-rich environment, inducing an inflammatory phenotype and anti-tumoral activity. The expression of CXCL9 and CXCL10 further supports lymphocyte recruitment, potentially facilitating greater lymphocyte infiltration and disrupting the immunosuppressive TME. This approach offers a promising strategy to improve immunotherapy outcomes in TNBC patients, particularly those with low immune cell infiltration, thereby addressing a critical unmet clinical need.
Published in
Macrophages expressing chimeric cytokine receptors have an inflammatory phenotype and antitumoral activity upon IL-10 or TGFβ stimulation
Traxel S, Schmidt F, Beerli C et al. · Journal for immunotherapy of cancer 2025 · PMID 41093623 · doi:10.1136/jitc-2024-011057
This dataset
Open GSE280810 in finder → Find more human RNA-seq datasets → Breast cancer landscape →
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 GSE280810_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 PRJNA1180581 and SRA study SRP542437. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41093623) ↗
Study design
30 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 30 sample titles: 30 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
More Breast cancer datasets

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