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Cytokine–ontogeny interaction shapes macrophage transcriptional states (combined GM-CSF– and M-CSF–derived macrophages)

ABSTRACT: We generated eight macrophage states using a cytokine–ontogeny matrix, combining two macrophage ontogenies (M-CSF and GM-CSF) with four cytokines (IL‑4, IFN‑γ, IL‑10, TGF‑β). Bulk RNA‑seq on five biological replicates per condition revealed that PC1 (54% variance) segregated ontogeny: GM‑CSF states loaded negatively, M‑CSF states positively. Gene‑set enrichment analysis of negative PC1 loadings highlighted NfkB programs, confirming the intrinsic inflammatory bias of GM‑CSF macrophages (Hamilton 2008; Hamilton et al. 2016)

ORGANISM(S): Mus musculus

PROVIDER: GSE304646 | GEO | 2025/09/30

REPOSITORIES: GEO

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Cytokine–ontogeny interaction shapes macrophage transcriptional states (GM-CSF–derived macrophages)

Project description:In GM-CSF–derived macrophages, bulk RNA-seq was performed on five biological replicates per cytokine condition (IL‑4, IFN‑γ, IL‑10, TGF‑β). IL‑4 separated along PC1 (47% variance) but showed no additional Hallmark enrichment. PC2 (25% variance) distinguished the IFN‑γ pole characterized by IRF1/STAT1-regulated genes (Gbp genes, Cxcl9), from IL‑4 and IL‑10/TGF‑β poles, denoting distinct remodeling programs. These data establish an ontogeny‑dependent divergence at the transcriptomic level.

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Cytokine–ontogeny interaction shapes macrophage transcriptional states

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Single-cell RNA-sequencing resolves IL-4 and IFN-γ into distinct inflammatory trajectories within GM-CSF macrophages

Project description:To account for the within-state heterogeneity of GM-CSF compared to M-CSF macrophages (Helft et al. 2015), we performed multiplexed scRNA-seq on 49,441 GM-CSF–derived macrophages stimulated with IL‑4, IFN‑γ, IL‑10, or TGF‑β. Cells were visualized by principal component analysis (PC1 = 13.21%, PC2 = 4.65%), which recapitulated patterns previously observed in bulk RNA-seq. IL‑4 displaced cells farthest along PC1 towards a cell cluster enriched for NfkB controlled gene expression with high Ccl22 and Ccr7, consistent with a dendritic‑cell‑like, T‑cell‑activating phenotype. IFN‑γ dominated PC2, retaining high MHC-II expression while adding a complement/interferon module (C1qb, C1qc, Gbp2, Irf1), and showed enrichment for IRF1/8 and STAT1 transcription factor signatures. TGF‑β and IL‑10 co-clustered in the PC1/PC2 low quadrant and shared expression of reparative markers including Chil3 and Cd24, forming an immunosuppressive, trophic branch distinct from either inflammatory pole. Together, these data show that within the GM-CSF lineage, IL‑4 and IFN‑γ drive orthogonal inflammatory trajectories, whereas IL‑10 and TGF‑β consolidate a shared remodeling program.

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Cytokine–ontogeny interaction shapes macrophage transcriptional states (combined GM-CSF– and M-CSF–derived macrophages)

Project description:Cytokine–ontogeny interaction shapes macrophage transcriptional states (combined GM-CSF– and M-CSF–derived macrophages)

| PRJNA1301986 | ENA

Cytokine–ontogeny interaction shapes macrophage transcriptional states (GM-CSF–derived macrophages)

Project description:Cytokine–ontogeny interaction shapes macrophage transcriptional states (GM-CSF–derived macrophages)

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miRNA expression microarrays in GM-CSF or GM-CSF+IL6-induced mouse MDSC

Project description:Myeloid-derived suppressor cells (MDSCs) have emerged as major regulators of immune responses in cancer and other pathological conditions. Multiple factors including cytokines, transcription factors and multiple signaling pathways are involved in MDSC differentiation. Cytokines such as granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin(IL-6) etc could in vitro mediate development of MDSCs.IL-6 with GM-CSF mediated MDSC not only had stronger suppressive function but also the dynamics of their suppressive function was different from GM-CSF alone mediated MDSCs.To found a new regulatory factor (s) in tumor and inflammatory environments, we compared GM-CSF and IL-6 mediated MDSCs with GM-CSF alone mediated MDSCs using lncRNA microarray, miRNA microarrays and protein-coding mRNA microarrays.

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2025-04-16 | GSE256208 | GEO

Effect of siRNA-mediated GSK3 knock-down on the transcriptional signature of human GM-CSF-dependent monocyte-derived macrophages

Project description:The functional versatility of macrophages is intrincately tied to factors such as their ontogeny and the specific tissue and extracellular environment. Monocyte-derived macrophages are oppositely instructed by M-CSF or GM-CSF. GM-CSF drives monocyte-derived macrophages towards heightened pro-inflammatory activity and the acquisition of the lung alveolar macrophage phenotype and gene profile whereas M-CSF gives rise to anti-inflammatory, pro-resolving, and immunosuppressive monocyte-derived macrophages. We explored the molecular impact of siRNA mediated knocking-down GSK3A, GSK3B or both (GSK3A/B) on the gene expression profile of GM-CSF-primed human monocyte derived macrophages. GSK3A/B knowdown skewed the transcriptional profile of GM-MØ towards an anti-inflammatory phenotype.

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Project description:Interleukin-21 (IL-21) has broad actions on T- and B-cells, but its actions in innate immunity are poorly understood. Here we show that IL-21 induced apoptosis of conventional dendritic cells (cDCs) via STAT3 and Bim, and this was inhibited by granulocyte-macrophage colony-stimulating factor (GM-CSF). ChIP-Seq analysis revealed genome-wide binding competition between GM-CSF-induced STAT5 and IL-21-induced STAT3. Expression of IL-21 in vivo decreased cDC numbers, and this was prevented by GM-CSF. Moreover, repetitive M-NM-1-galactosylceramide injection of mice induced IL-21 but decreased GM-CSF production by natural killer T (NKT) cells, correlating with decreased cDC numbers. Furthermore, adoptive-transfer of wild-type CD4+ T cells caused more severe colitis with increased DCs and interferon (IFN)-M-NM-3-producing CD4+ T cells in Il21r-/-Rag2-/- mice (which lack T cells and have IL-21-unresponsive DCs) than in Rag2-/- mice. Thus, IL-21 and GM-CSF exhibit cross-regulatory actions on gene regulation and apoptosis, regulating cDC numbers and thereby the magnitude of the immune response. Total 6 samples were examined. Splenic dendritic cells were treated with IL-21 and/or GM-CSF studying STAT3 and STAT5B binding in the genome

2013-02-14 | E-GEOD-27161 | biostudies-arrayexpress

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