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Microarray Analysis of miRNA Expression Profiles in Monocytic Myeloid-derived Suppressor Cells in Echinococcus granulosus-infected mice

ABSTRACT: To investigate the miRNA expression profiles in the splenic M-MDSCs of normal and Eg-psc-infected mice, and performed bioinformatics analysis of the differentially expressed miRNAs to explore the possible biological processes and pathways associated with M-MDSCs.

ORGANISM(S): Mus musculus

PROVIDER: GSE110187 | GEO | 2019/12/23

REPOSITORIES: GEO

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Microarray Analysis of LncRNA Expression Profiles in Monocytic Myeloid-derived Suppressor Cells in Echinococcus granulosus-infected mice

Project description:To investigate the lncRNA and mRNA expression profiles in the splenic M-MDSCs of normal and Eg-psc-infected mice, and performed bioinformatics analysis of the differentially expressed lncRNAs to explore the possible biological processes and pathways associated with M-MDSCs.

2019-12-23 | GSE110253 | GEO

Microarray Analysis of Expression Profiles in Monocytic Myeloid-derived Suppressor Cells in Echinococcus granulosus-infected mice

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Microarray analysis of long non-coding RNA expression profiles in monocytic myeloid-derived suppressor cells in Echinococcus granulosus-infected mice.

Project description:BACKGROUND:Cystic echinococcosis is a worldwide chronic zoonotic disease caused by infection with the larval stage of Echinococcus granulosus. Previously, we found significant accumulation of myeloid-derived suppressor cells (MDSCs) in E. granulosus infection mouse models and that they play a key role in immunosuppressing T lymphocytes. Here, we compared the long non-coding RNA (lncRNA) and mRNA expression patterns between the splenic monocytic MDSCs (M-MDSCs) of E. granulosus protoscoleces-infected mice and normal mice using microarray analysis. METHODS:LncRNA functions were predicted using Gene Ontology enrichment and the Kyoto Encyclopedia of Genes and Genomes pathway analysis. Cis- and trans-regulation analyses revealed potential relationships between the lncRNAs and their target genes or related transcription factors. RESULTS:We found that 649 lncRNAs were differentially expressed (fold change ? 2, P < 0.05): 582 lncRNAs were upregulated and 67 lncRNAs were downregulated; respectively, 28 upregulated mRNAs and 1043 downregulated mRNAs were differentially expressed. The microarray data was validated by quantitative reverse transcription-PCR. The results indicated that mRNAs co-expressed with the lncRNAs are mainly involved in regulating the actin cytoskeleton, Salmonella infection, leishmaniasis, and the vascular endothelial growth factor (VEGF) signaling pathway. The lncRNA NONMMUT021591 was predicted to cis-regulate the retinoblastoma gene (Rb1), whose expression is associated with abnormal M-MDSCs differentiation. We found that 372 lncRNAs were predicted to interact with 60 transcription factors; among these, C/EBP? (CCAAT/enhancer binding protein beta) was previously demonstrated to be a transcription factor of MDSCs. CONCLUSIONS:Our study identified dysregulated lncRNAs in the M-MDSCs of E. granulosus infection mouse models; they might be involved in M-MDSC-derived immunosuppression in related diseases.

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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.

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

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

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