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The mRNA levels of Ly6G+ cells from the bone marrow of septic mice after IFN-gamma stimulation.

ABSTRACT: Currently, immunotherapy represents a promising therapeutic approach for patients with sepsis in the refractory immunosuppressive phase. The pro-inflammatory cytokine interferon-gamma (IFN-γ) has been investigated in both septic patients and murine sepsis models, yet no significant mortality reduction has been reported in clinical applications. We hypothesize that IFN-γ treatment may concurrently activate polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs), a population of immunosuppressive cells, during the immunocompromised phase of sepsis. To investigate this mechanism, we stimulated bone marrow cells from CLP (cecal ligation and puncture) model mice in the immunosuppressive phase of sepsis with IFN-γ in vitro. Subsequently, we isolated PMN-MDSCs and performed RNA sequencing to analyze transcriptomic alterations at the gene expression level.

ORGANISM(S): Mus musculus

PROVIDER: GSE297320 | GEO | 2026/05/15

REPOSITORIES: GEO

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Project description:Myeloid-derived suppressor cells (MDSCs) are key players in immune evasion, tumor progression and metastasis. MDSCs accumulate under various pathological states, and fall into two functionally and phenotypically distinct subsets: polymorphonuclear (PMN)-MDSCs and monocytic (M)-MDSCs. These subsets have been studied extensively in humans and mice, yet to date no study has identified MDSC subsets in dogs with spontaneous tumors. As dogs are an excellent model for human tumor development and progression, we set out to identify PMN-MDSCs and M-MDSCs in clinical canine oncology patients. We identified MDSCs as hypodense MHC class II-CD5-CD21-CD11b+ cells and show for the first time that they can also be subdivided into polymorphonuclear (CADO48A+CD14-) and monocytic (CADO48A-CD14+) subsets. The transcriptomic signatures of PMN-MDSCs and M-MDSCs are distinct from each other and from those of conventional polymorphonuclear (PMN) and monocytic cells, respectively. Notably, bioinformatic analyses reveal a statistically significant similarity between canine and previously published human MDSC gene expression patterns. As in humans, peripheral blood frequencies of canine PMN-MDSCs and M-MDSCs are significantly different in dogs with cancer compared to healthy control dogs (PMN-MDSCs: p < .001; M-MDSCs: p < .01). Furthermore, a comparison of our canine MDSC RNA-seq data with transcriptomic results previously published for human and murine MDSCs highlights five commonly upregulated genes in PMN-MDSCs in all species, suggesting that these genes are evolutionarily conserved and functionally important. Interestingly, one gene has previously been implicated in PMN-MDSC function (MMP8), but four genes (LTF, LCN2, CAMP, EBP41L3) are novel in the context of PMN-MDSCs. Our findings therefore demonstrate for the first time that dogs have two distinct populations of MDSCs, characterized by specific phenotypic and transcriptomic signatures that share key features of human MDSC subsets. Importantly, by leveraging the power of evolution, we have identified additional conserved genes in PMN-MDSCs of multiple species which may play a role in MDSC function. Our findings therefore validate the dog as a model for studying MDSCs in the context of cancer.

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The mRNA levels of Ly6G+ cells from the bone marrow of septic mice after IFN-gamma stimulation.

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