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A new soluble CSF1R-dimeric mutein with enhanced trapping of both CSF-1 and IL-34 reduces suppressive tumor-associated macrophages in mesothelioma.

GSE282239 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2025/03/26 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 12 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
MesotheliomaThis series is part of our curated briefing on it.
Samples
12 samples: 3 × Meso13 cells, MCTS vs 3 × Meso13 cells + mono, MCTS vs 3 × Meso34 cells, MCTS vs 3 × Meso34 cells + mono, MCTSGroups 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
New soluble CSF-1R-dimeric mutein with enhanced trapping of both CSF-1 and IL-34 reduces suppressive tumor-associated macrophages in pleural mesotheliomaJournal for immunotherapy of cancer · 2025
Summary (written by the submitters)
Background: Signalling through the colony stimulating factor-1 receptor (CSF-1R) upon binding of its ligands CSF-1 and IL-34 has tumorigenic effects in several cancers through both induction of suppressive macrophages, and survival/proliferation of tumor cells. In addition, IL-34 tumorigenic effect can also be mediated by signalling through its other receptors, protein-tyrosine phosphatase zeta (PTPzeta), Syndecan-1 (CD138) and triggering receptor expressed on myeloid cells 2 (TREM2).
Read the full summary ↓
Inhibition of CSF-1R signalling with small tyrosine kinase inhibitors or neutralization of CSF-1 and/or IL-34 using antibodies have been proposed to be used in cancer but their effect is limited, they have drawbacks since they only partially inhibit CSF-1 or IL-34 activity and in the case of small tyrosine kinase inhibitors lead to secondary effects due to lack of specificity. Thus, there is a need for a more specific and yet integrative approach. Methods: A human mutated form of the extracellular portion of CSF-1R was in silico modelized to trap both IL-34 and CSF-1 with higher affinity than the wild-type CSF-1R by replacing the methionine residue at position 149 by a Lysine (M149K). The extracellular portion of the mutated CSF-1R M149K was dimerized using the immunoglobulin Fc sequence of a silent human IgG1 (sCSF-1RM149K-Fc). Signalling through CSF-1R, survival of monocytes and differentiation of suppressive macrophages were analyzed using mesothelioma patient’s samples and mesothelioma/macrophage spheroids in the presence of sCSF-1RM149K-Fc or sCSF-1R-Fc wild type control (sCSF-1RWT-Fc). Results: We defined that the D1 to D5 domains of the extracellular portion of CSF-1R were required for efficient binding to IL-34 and CSF-1. The mutein sCSF-1RM149K-Fc trapped with higher affinity than sCSF-1RWT-Fc both recombinant CSF-1 and IL-34 added in culture and naturally produced in mesothelioma pleural effusions. This was shown by inhibition of CSF-1R signalling, survival and differentiation of human suppressive macrophage in vitro and in vivo induced by mesothelioma cells. Neutralization of IL-34 and CSF-1 resulted in higher killing of mesothelioma cells by a tumor-specific CD8+ T cell clone in mesothelioma/macrophage spheroids. Conclusions: sCSF-1RM149K-Fc efficiently inhibited CSF-1R signalling, monocyte survival and suppressive macrophage differentiation induced by mesothelioma cells producing CSF-1 and IL-34 as well as restored cytotoxic T cell responses. sCSF-1RM149K-Fc efficiently and simultaneously trap both CSF-1 and IL-34 with high therapeutic potential versus other therapies under development targeting single components of this complex cytokine pathway involved in cancer.
Published in
New soluble CSF-1R-dimeric mutein with enhanced trapping of both CSF-1 and IL-34 reduces suppressive tumor-associated macrophages in pleural mesothelioma
Joalland N, Quéméner A, Deshayes S et al. · Journal for immunotherapy of cancer 2025 · PMID 40101804 · doi:10.1136/jitc-2024-010112
This dataset
Open GSE282239 in finder → Find more human RNA-seq datasets → Mesothelioma 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 GSE282239_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 PRJNA1187633 and SRA study SRP546033. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40101804) ↗
Study design
3 × Meso13 cells, MCTS vs 3 × Meso13 cells + mono, MCTS vs 3 × Meso34 cells, MCTS vs 3 × Meso34 cells + mono, MCTS

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 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
More Mesothelioma datasets

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.