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Autophagic monocytic myeloid-derived suppressor cells protect mice cardiac allografts

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

PROVIDER: PRJNA705095 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13790600_1.fastq.gz	Fastqsanger.gz
	SRR13790600_2.fastq.gz	Fastqsanger.gz
	SRR13790601_1.fastq.gz	Fastqsanger.gz
	SRR13790601_2.fastq.gz	Fastqsanger.gz
	SRR13790596_1.fastq.gz	Fastqsanger.gz

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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

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

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

mTOR masters monocytic myeloid-derived suppressor cells in mice with allografts or tumors.

Project description:CD11b(+) Gr1(+) myeloid-derived suppressor cells (MDSCs) play critical roles in controlling the processes of tumors, infections, autoimmunity and graft rejection. Immunosuppressive drug rapamycin (RPM), targeting on the key cellular metabolism molecule mTOR, is currently used in clinics to treat patients with allo-grafts, autoimmune diseases and tumors. However, the effect of RPM on MDSCs has not been studied. RPM significantly decreases the cell number and the immunosuppressive ability on T cells of CD11b(+) Ly6C(high) monocytic MDSCs (M-MDSCs) in both allo-grafts-transplanted and tumor-bearing mice respectively. Mice with a myeloid-specific deletion of mTOR have poor M-MDSCs after grafting with allo-skin tissue or a tumor. Grafting of allo-skin or tumors significantly activates glycolysis pathways in myeloid precursor cells in bone marrow, which is inhibited by RPM or mTOR deletion. 2-deoxyglucose (2-DG), an inhibitor of the glycolytic pathway, inhibits M-MDSC differentiation from precursors, while enhancing glycolysis by metformin significantly rescues the RPM-caused deficiency of M-MDSCs. Therefore, we offer evidence supporting that mTOR is an intrinsic factor essential for the differentiation and immunosuppressive function of M-MDSCs and that these metabolism-relevant medicines may impact MDSCs-mediated immunosuppression or immune tolerance induction, which is of considerable clinical importance in treating graft rejection, autoimmune diseases and cancers.

| S-EPMC4735296 | 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

The mTOR Deficiency in Monocytic Myeloid-Derived Suppressor Cells Protects Mouse Cardiac Allografts by Inducing Allograft Tolerance.

Project description:BackgroundMyeloid-derived suppressor cells (MDSCs) can prevent allograft rejection and induce immune tolerance in transplantation models. Previous studies have demonstrated that inhibition of mTOR signaling can enhance the MDSC protective effect in heart transplantation (HTx) by promoting MDSC expansion. In addition, mTOR inhibition is related to autophagy. The present study investigated the protective mechanism of mTOR-deficient monocytic MDSCs (M-MDSCs) in mouse HTx.MethodsMyeloid-specific mTOR conditional knockout mice were generated to obtain mTOR-/- M-MDSCs. The proliferation and immunosuppressive function of mTOR-/- M-MDSCs were determined by flow cytometry and T cell proliferation assays. The mTOR-/- M-MDSC intracellular autophagy levels were determined using western blotting and electron microscopy. RNAseq analysis was performed for wild-type (WT) and mTOR-/- M-MDSCs. Allogeneic HTx mouse model was established and treated with WT or mTOR-/- M-MDSCs. Enzyme-linked immunosorbent assay, flow cytometry, and immunohistochemistry assays were performed to determine WT and mTOR-/- M-MDSC-induced immune tolerance.ResultsThe mTOR deficiency promoted M-MDSC differentiation and enhanced intracellular autophagy levels in vivo and in vitro. mTOR deficiency also enhanced the immunosuppressive function of M-MDSCs. In addition, infusing with WT and mTOR-/- M-MDSCs prolonged cardiac allograft survival and established immune tolerance in recipient mice by inhibiting T cell activation and inducing regulatory T cells.ConclusionmTOR deficiency enhances the immunosuppressive function of M-MDSCs and prolongs mouse cardiac allograft survival.

| S-EPMC8062712 | biostudies-literature

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

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

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Monocytic-Myeloid Derived Suppressor Cells Suppress T-Cell Responses in Recovered SARS CoV2-Infected Individuals

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

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