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Distinct population of immune suppressive macrophages differentiate from monocytic myeloid-derived suppressor cells in cancer

ABSTRACT: Distinct population of immune suppressive macrophages differentiate from monocytic myeloid-derived suppressor cells in cancer

PROVIDER: PRJNA681580 | ENA |

REPOSITORIES: ENA

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Distinct population of immune suppressive macrophages differentiate from monocytic myeloid-derived suppressor cells in cancer

Project description:Here, we report that functional heterogeneity of macrophages in cancer could be determined by the nature of their precursors: monocytes (Mon) and monocytic myeloid-derived suppressor cells (M-MDSC). Macrophages differentiated from M-MDSC, but not from Mon were immune suppressive with genomic profile matching that of M-MDSC. Immune suppressive activity of M-MDSC derived macrophages was dependent on the persistent expression of S100A9 protein in these cells. S100A9 also promoted M2 polarization of macrophages. Tissue resident and Mon derived macrophages lacked expression of this protein. S100A9 dependent immune suppressive activity of macrophage was mediated via transcription factor CEBP/β. The presence of S100A9 positive macrophages in tumor tissues was associated with shorter survival in patients with head and neck cancer and poor response to PD-1 antibody treatment in patients with metastatic melanoma. Thus, this study revealed the pathway of the development of immune suppressive macrophages and suggested approach to their selective targeting.

2020-12-14 | GSE162353 | GEO

Myeloid-derived Suppressor Cells in Colorectal Cancer

Project description:The aim of the study is to evaluate whether the preoperative level of myeloid-derived suppressor cells is associated with postoperative complications classified by Clavien-Dindo categories. Levels of all MDSC, polymorphonuclear MDSC (PMNMDSC), monocytic MDSC (MMDSC), early-stage MDSC (EMDSC) and monocytic to polymorphonuclear MDSC ratio (M/PMN MDCS) were established and compared in patients with postoperative complications, severe postoperative complications (>= IIIA according to Clavien-Dindo) and severe septic complications.

| 2381881 | ecrin-mdr-crc

Distinct Populations of Immune-Suppressive Macrophages Differentiate from Monocytic Myeloid-Derived Suppressor Cells in Cancer.

Project description: Not available

| S-EPMC7809772 | biostudies-literature

Monocytic myeloid-derived suppressor cells accumulate in the lungs of influenza A virus-infected mice

Project description:Influenza A virus (IAV) infection causes an acute respiratory disease characterized by a strong inflammatory immune response and severe immunopathology. Pro-inflammatory mechanisms are well described in the murine IAV infection model, but less is known about the mechanisms leading to the resolution of inflammation. Here, we analyzed the contribution of monocytic myeloid-derived suppressor cells (mono-MDSC) to this process. An accumulation of mono-MDSC within the lungs was observed during the course of IAV infection and phenotypic characterization of these mono-MDSC by flow cytometry and RNA-Seq revealed an activated phenotype showing both pro- and anti-inflammatory features, including the expression of iNOS by a fraction of cells in an IFN-g-dependent manner. Mono-MDSC isolated from lungs of IAV-infected animals displayed suppressive activity when tested in vitro, and iNOS inhibitors could abrogate this suppressive activity. Collectively, our data suggest that during IAV infection monocytes can differentiate into mono-MDSC, which might contribute to the prevention of immunopathology during this life-threatening disease.

2015-10-01 | GSE62795 | GEO

Transcriptome analysis of p16/p21-dependent monocytic myeloid-derived suppressor cells accumulation.

Project description:p16 and p21 act as tumor suppressors through induction of cellular senescence. However, senescence-independent roles of these CDK inhibitors are not known. To identify the mechanism responsible for the failure of Mo-MDSCs (monocytic myeloid-derived suppressor cells) infiltration into tumor allografts in p16/p21-double knockout (DKO) mice, we searched for chemokine receptors that were highly expressed in Mo- but not PMN-MDSCs (polymorphonuclear myeloid-derived suppressor cells) and were downregulated in p16/p21-DKO as compared to WT Mo-MDSCs. Ccr2, Ccr5, and Cx3cr1 were identified by RNA-seq analysis.

2018-02-13 | GSE93359 | GEO

Autophagic monocytic myeloid-derived suppressor cells protect mice cardiac allografts

Project description:Autophagic monocytic myeloid-derived suppressor cells protect mice cardiac allografts

| PRJNA705095 | ENA

Cisplatin inhibits frequency and suppressive activity of monocytic myeloid-derived suppressor cells in cancer patients.

Project description: Not available

| S-EPMC8237969 | biostudies-literature

Identification of the networks that regulate human monocytic myeloid-derived suppressor cell differentiation into inflammatory macrophages

Project description:Background: Monocytic myeloid-derived suppressor cells (mMDSC) support immune evasion of tumors by blocking tumoricidal T and NK cell response. Efforts to reverse mMDSC-mediated immunosuppression identified that the TLR7/8 agonist R848 induces their maturation into tumoricidal macrophages Purpose: The factors that determine whether human mMDSC differentiate into MACinflam or MACsuppress are unclear. To investigate this issue, the role of cytokines and genes activated following R848 treatment was examined. Methods: After 4 hour stimulation, cells from stimulated mMDSC were stored in RNA protect (Qiagen, Frederick, MD). Total RNA was isolated using the RNeasy micro kit (Qiagen) and RNA quality was assessed using an Agilent 2200 TapeStation. mRNA libraries were generated using the Smart-Seq ultra-low input kit (Clontech) and sequenced using a HiSeq2500 sequencer using IlluminaTruSeq v4 chemistry with 125bp paired-end reads. Sequences were aligned to the human (hg19) reference genome. Genes that were differentially expressed compared to untreated samples were identified using CLC genomics workbench (version 10). Results: TNFa combined with IL-6 effectively supports the differentiation of mMDSC into tumoricidal macrophage by activating expression of conserved set of genes. Mechanistically, transcription factors NF-KB and STAT4 emerge as important regulators and potential targets to modify mMDSC behavior.

2017-10-19 | GSE105142 | GEO

Expression data from monocytes and monocytic myeloid-derived suppressor cells from HNSCC patients and healthy donors [RNA-seq]

Project description:A better understanding of the mechanisms that induce and drive human suppressive myeloid cells, such as myeloid-derived suppressor cells (MDSCs) and tolerogenic dendritic cells (TolDCs), stimulates therapeutic approaches that intent to restore the immune balance in patients. Here, we compared gene profiles of in vitro generated and isolated M-MDSCs derived from cancer patients to monocytes isolated from cancer patients and healthy donors.

2021-11-11 | GSE183854 | GEO

Immune suppressive activity of myeloid-derived suppressor cells in cancer requires inactivation of the type I interferon pathway

Project description:Myeloid-derived suppressor cells (MDSC) are pathologically activated neutrophils and monocytes with potent immune suppressive activity. These cells play an important role in accelerating tumor progression and undermining the efficacy of anti-cancer therapies. The natural mechanisms limiting MDSC activity are not well understood. Here, we present evidence that type I interferons (IFN1) receptor signaling serves as a universal mechanism that restricts acquisition of suppressive activity by these cells. Downregulation of the IFNAR1 chain of this receptor was found in MDSC from cancer patients and mouse tumor models. The decrease in IFNAR1 depended on the activation of the p38 protein kinase and was required for activation of the immune suppressive phenotype. Whereas deletion of IFNAR1 was not sufficient to convert neutrophils and monocytes to MDSC, genetic stabilization of IFNAR1 in tumor bearing mice undermined suppressive activity of MDSC and had potent antitumor effect. Stabilizing IFNAR1 using inhibitor of p38 combined with the interferon induction therapy elicited a robust anti-tumor effect. Thus, negative regulatory mechanisms of MDSC function can be exploited therapeutically.

2021-02-15 | GSE166770 | GEO

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