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Tumor-infiltrating Monocytic Myeloid-derived suppressor cells play a key role in forming immunosuppressive microenvironment in human gastric cancer

ABSTRACT: The present data suggest that M-MDSC, play a predominant role in forming the immunosuppressive microenvironment in GC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE231539 | GEO | 2024/01/22

REPOSITORIES: GEO

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Tumor-infiltrating monocytic myeloid-derived suppressor cells contribute to the development of an immunosuppressive tumor microenvironment in gastric cancer

Project description:The present study suggests that TI-M-MDSCs, especially IER3+ ones, may play a predominant role in the development of the immunosuppressive and ICI-resistant GC TIME.

2024-01-22 | GSE201347 | GEO

Tumor-infiltrating Monocytic Myeloid-derived suppressor cells play a key role in forming immunosuppressive microenvironment in human gastric cancer

Project description:Tumor-infiltrating Monocytic Myeloid-derived suppressor cells play a key role in forming immunosuppressive microenvironment in human gastric cancer

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Modified method for differentiation of myeloid-derived suppressor cells in vitro enhances immunosuppressive ability via glutathione metabolism

Project description:Myeloid-derived suppressor cells (MDSCs), which accumulate in tumor bearers, are known to suppress anti-tumor immunity and thus promote tumor progression. MDSCs are considered a major cause of resistance against immune checkpoint inhibitors in patients with cancer. Therefore, MDSCs are potential targets in cancer immunotherapy. In this study, we modified an in vitro method of MDSC differentiation. Upon stimulating bone marrow (BM) cells with granulocyte-macrophage colony-stimulating factor in vitro, we obtained both lymphocyte antigen 6G positive (Ly-6G+) and negative (Ly-6G−) MDSCs (collectively, hereafter referred to as conventional MDSCs), which were non-immunosuppressive and immunosuppressive, respectively. We then found that MDSCs differentiated from Ly-6G− BM (hereafter called 6G− BM-MDSC) suppressed T-cell proliferation more strongly than conventional MDSCs, whereas the cells differentiated from Ly-6G+ BM (hereafter called 6G+ BM-MDSC) were non-immunosuppressive. In line with this, conventional MDSCs or 6G− BM-MDSC, but not 6G+ BM-MDSC, promoted tumor progression in tumor-bearing mice. Moreover, we identified that activated glutathione metabolism was responsible for the enhanced immunosuppressive ability of 6G− BM-MDSC. Finally, we showed that Ly-6G+ cells in 6G− BM-MDSC, which exhibited weak immunosuppression, expressed higher levels of Cybb mRNA, an immunosuppressive gene of MDSCs, than 6G+ BM-MDSC. Together, these data suggest that the depletion of Ly-6G+ cells from the BM cells leads to differentiation of immunosuppressive Ly-6G+ MDSCs. In summary, we propose a better method for MDSC differentiation in vitro. Moreover, our findings contribute to the understanding of MDSC subpopulations and provide a basis for further research on MDSCs.

2023-01-10 | GSE218704 | GEO

ILT3 (LILRB4) Promotes the Immunosuppressive Function of Tumor-Educated Human Monocytic Myeloid-Derived Suppressor Cells

Project description:Myeloid-derived suppressor cells (MDSCs) are immature myeloid cells that accumulate in the tumor microenvironment (TME). MDSCs have been shown to dampen anti-tumor immune responses and promote tumor growth; however, the mechanisms of MDSC induction and their role in promoting immune suppression in cancer remain poorly understood. Here, we characterized the phenotype and function of monocytic MDSCs (M-MDSCs) generated by co-culture of human peripheral blood mononuclear cells with SK-MEL-5 cancer cells in vitro. We selected the SK-MEL-5 human melanoma cell line to generate M-MDSCs because these cells form subcutaneous tumors rich in myeloid cells in humanized mice. M-MDSCs generated via SK-MEL-5 co-culture expressed low levels of human leukocyte antigen (HLA)-DR, high levels of CD33 and CD11b and suppressed both CD8+ T cell proliferation and IFN-γ secretion. M-MDSCs also expressed higher levels of immunoglobulin-like transcript 3 (ILT3, also known as LILRB4) and immunoglobulin-like transcript 4 (ILT4, also known as LILRB2) on the cell surface compared to monocytes. We, therefore, investigated how ILT3 targeting could modulate M-MDSC cell function. Treatment with an anti-ILT3 antibody impaired the acquisition of the M-MDSC suppressor phenotype and reduced the capacity of M-MDSCs to cause T cell suppression. Finally, in combination with anti-programmed cell death protein 1 (PD1), ILT3 blockade enhanced T cell activation as assessed by IFN-γ secretion. These results suggest that ILT3 expressed on M-MDSCs has a role in inducing immunosuppression in cancer and that antagonism of ILT3 may be useful to reverse the immunosuppressive function of M-MDSCs and enhance the efficacy of immune checkpoint inhibitors.

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Tumor-infiltrating monocytic myeloid-derived suppressor cells mediate CCR5-dependent recruitment of regulatory T cells favoring tumor growth

Project description:Analysis of MDSC subsets from naive blood and RMA-S blood and RMA-S tumor, respectively. Tumor-infiltrating MO-MDSCs changed their expression pattern compared to blood and exhibited high levels of chemokines Total RNA obtained from PMN-MDSCs and MO-MDSCs from naive blood or from blood and tumor of RMA-S bearing mice

2012-10-17 | E-GEOD-41620 | biostudies-arrayexpress

Tumor-infiltrating monocytic myeloid-derived suppressor cells contribute to the development of an immunosuppressive tumor microenvironment in gastric cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-01-19 | GSE231540 | GEO

Exportin 1 governs the immunosuppressive functions of tumor myeloid derived suppressor cells through ERK1/2 nuclear export

Project description:Myeloid derived suppressor cells (MDSCs) are a main driver of immunosuppression in tumors. Understanding the mechanisms that determine the development and immunosuppressive function of these cells could provide new therapeutic targets to improve anti-tumor immunity. Here, we discovered in preclinical murine models, that exportin 1 (XPO1) expression is upregulated in tumor MDSCs and this expression is induced by IL-6 activated STAT3 during MDSC differentiation. XPO1 blockade transforms MDSCs into T cell-activating neutrophil-like cells, enhancing the anti-tumor immune response and restraining tumor growth. Mechanistically, XPO1 inhibition leads to nuclear entrapment of ERK1/2, resulting in prevention of ERK1/2 phosphorylation post-IL-6 activation of the MAPK signaling pathway. Similarly, XPO1 blockade in human MDSCs induces neutrophil-like cells with immunostimulatory functions. Therefore, our findings have revealed a critical role of XPO1 in MDSC differentiation and suppressive function; exploiting these new discoveries reveals new targets to reprogram immunosuppressive MDSCs to improve cancer therapeutic responses.

2024-06-30 | GSE269677 | GEO

Tumor-infiltrating monocytic myeloid-derived suppressor cells mediate CCR5-dependent recruitment of regulatory T cells favoring tumor growth

2012-10-17 | GSE41620 | GEO

RNA sequencing of CHBP- and CHBP+ monocyte myeloid-derived suppressor cells

Project description:MDSC (myeloid-derived suppressor cells) can be divided into two subsets: granulocytic MDSC (G-MDSC) and monocyte MDSC (M-MDSC).We found that CHBP induced M-MDSC have stronger immunosuppressive function. To identify the specific role of CHBP induced M-MDSC, we used RNA squencing to compare the M-MDSC with CHBP induced M-MDSC. We analyzed the differential expressed genes between these two groups.

2020-11-05 | GSE160822 | GEO

Autophagic monocytic myeloid-derived suppressor cells protect mice cardiac allografts

Project description:Background: Myeloid-derived suppressor cells (MDSCs) could prevent allograft rejections and induce immune tolerance in transplantation models. Previous studies demonstrated that inhibition of mTOR signal could enhance MDSCs protective effect in cardiac transplantation model via promoting MDSCs expansion. And the inhibition of mTOR is related with autophagy. Herein, this study was designed to investigate the protective mechanism of mTOR deficiency M-MDSCs in cardiac transplantation model. Methods: Myeloid-specific mTOR conditional knockout mice were generated to get mTOR deficiency M-MDSCs. The proliferation and immunosuppressive function of mTOR deficiency M-MDSCs were determined by flow cytometry and CFSE T cell proliferation assays. mTOR deficiency M-MDSCs intracellular autophagy levels were determined by western blot and Electron microscopy. RNAseq analysis was performed for WT and mTOR-deficient M-MDSC cells. Cervical cardiac transplantation model mice were generated. ELISA were performed for control mice, model mice, WT MDSCs infusion model mice and mTOR-deficient MDSCs infusion model mice to examine the inflammatory cytokines in the recipients mice serum. Flow cytometry and immunohistochemistry were performed to determine mTOR-deficient MDSCs induced immune tolerance. Results: mTOR deficiency could promote M-MDSCs differentiation and enhance intracellular autophagy levels in vivo and in vitro. mTOR deficiency also enhance the immunosuppressive function of M-MDSCs. In addition, infusing mTOR deficiency M-MDSCs could also prolong cardiac allograft survival and establish immune tolerance in recipient mice by inhibiting T cell activation and inducing Tregs. Conclusion: mTOR-deficiency enhances M-MDSCs cells autophagy and immunosuppressive function and prolongs mice cardiac allograft survival.

2021-02-27 | GSE167594 | GEO

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