ArticleFrontiers in immunology2026
Single-cell and spatial profiling reveal an IL-10-associated iCAF-M2 macrophage communication axis in high-grade serous ovarian cancer ascites.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
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Abstract
Aims and objectives: High-grade serous ovarian cancer (HGSOC) ascites represents a highly immunosuppressive tumour microenvironment characterized by complex stromal-immune interactions. In this study, we aimed to delineate the cellular communication networks shaping immune dysfunction within HGSOC ascites, identify key regulatory signalling pathways, characterize the fibroblast-macrophage axis at single-cell resolution, and evaluate the therapeutic potential of IL-10 blockade in reversing macrophage-mediated immunosuppression. Methods: Single-cell RNA sequencing data of eight ascites samples from six HGSOC patients (GSE146026) were analysed using Seurat for clustering and differential expression, followed by CellChat to infer ligand-receptor communication. Sub-clustering defined inflammatory CAFs (iCAF), myofibroblast CAFs (mCAF), and macrophage subtypes (M1/M2). GO/KEGG enrichment assessed functional pathways. Multiplex immunofluorescence validated spatial interactions of IL10+ iCAF and IL10RA+ macrophages in patient tissues. An immune-humanized patient-derived xenograft (PDX) mouse model was established to evaluate the therapeutic effect of IL-10 blockade. Results: Single-cell transcriptomic analysis of HGSOC ascites revealed macrophages and cancer-associated fibroblasts as dominant cell populations within the tumour microenvironment. Cell-cell communication analysis identified IL-10-IL-10RA signalling as a prominent interaction pathway linking inflammatory CAFs (iCAFs) with M2-like macrophages. iCAFs displayed elevated IL-10 expression, while M2 macrophages showed increased IL-10RA/IL-10RB expression and were associated with exhausted immune states. Multiplex immunofluorescence confirmed spatial proximity between IL-10 Conclusion: This study identifies an IL-10-dependent iCAF-M2 macrophage immunoregulatory circuit as a central mechanism driving immune suppression in HGSOC. Targeting the IL-10 pathway effectively reverses M2 polarization and suppresses tumour progression, highlighting IL-10 blockade as a promising therapeutic strategy in ovarian cancer.
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