Whole genome expression profile of human decidual PMN-MDSC in normal pregnancy and unexplained recurrent pregnancy loss
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ABSTRACT:
PROVIDER: PRJNA578703 | ENA |
REPOSITORIES: ENA
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Project description:Polymorphonuclear myeloid-derived suppressor cell (PMN-MDSC) accumulate in maternal-fetal interface during pregnancy and play a role in maintenance of immune tolerance. Decreased PMN-MDSC is associated with pregnancy complications such as unexplained recurrent pregnancy loss (URPL). Whether PMN-MDSC function is different between normal pregnancy (NP) and URPL remains unexplored. Here we performed whole genome expression profile of 3 decidual PMN-MDSC from normal early pregnancy and 3 decidual PMN-MDSC from URPL. Total RNA were extracted. Cy5-labeled aRNA was hybridized and scanned on a G2505C Agilent Microarray Scanner with Agilent 0.1 XDR software. The gene expression pattern of the PMN-MDSC was significantly different between the NP group and the URPL group.
2020-06-30 | GSE139180 | GEO
Project description:It is suggested that decidual polymorphonuclear myeloid-derived suppressor cell (PMN-MDSCs) are a group of activated suppressive neutrophils. Decidual microenvironment can facilitate circulating neutrophils with phenotypes and functions of PMN-MDSCs. The mechanism of PMN-MDSCs differentiation induced by decidual microenvironment has not been fully understood. Here we performed whole genome expression profile of 3 decidual PMN-MDSCs and autologous neutrophils from normal early pregnancy. Total RNA were extracted. The arrays were scanned by the Agilent Scanner G2505C. There were differences of gene expression pattern between decidual PMN-MDSCs and autologous neutrophils in early normal pregnancy.
2022-05-13 | GSE192850 | GEO
Project description:Whole genome expression profile of human decidual PMN-MDSC and autologous neutrophils in normal pregnancy
| PRJNA793446 | ENA
Project description:Polymorphonuclear myeloid-derived suppressor cell (PMN-MDSC), also named pathologically activated neutrophil, is a critical component of tumor microenvironment (TME), playing crucial roles in tumor progression and therapy resistance. CD300ld is specifically expressed in normal neutrophils and is upregulated in PMN-MDSCs upon tumor bearing. CD300ld knockout (KO) inhibits the development of multiple tumor types in a PMN-MDSC-dependent manner. Here, we compared the transcriptome of PMN-MDSCs from WT mice and CD300ld KO mice.
2023-06-26 | GSE199602 | GEO
Project description:Myeloid-derived suppressor cells (MDSC), especially polymorphonuclear MDSC (PMN-MDSC), accumulate in maternal-fetal interface during pregnancy and are involved in the maintenance of immune tolerance. Decreased PMN-MDSC is associated with pregnancy complications such as unexplained recurrent pregnancy loss (URPL). In the present study we showed decreased PMN-MDSC in the URPL group compared with the normal pregnancy (NP) group, and PMN-MDSC was the major subset of MDSC in human decidua with potent immune suppression activity. We then performed gene expression profile and found that human decidual PMN-MDSC in the NP and URPL groups showed different gene and pathway signature, including apoptosis. Apoptosis of decidual PMN-MDSC was mediated by TNF-related apoptosis-induced ligand (TRAIL) in a Caspase 3 dependent manner. TRAIL was expressed in decidua and upregulated in decidua of the URPL group. Notably, of all the membrane TRAIL receptors, only DcR2 was down-regulated in PMN-MDSC in the URPL group. In vitro experiment demonstrated that DcR2 blockade sensitized PMN-MDSC to TRAIL-mediated apoptosis. Together, these data indicate that increased TRAIL and reduced DcR2 on PMN-MDSC sensitize PMN-MDSC response to TRAIL-induced apoptosis in the URPL group, which is responsible for decreased accumulation of PMN-MDSC in URPL.
| S-EPMC7338483 | biostudies-literature
Project description:Polymorphonuclear myeloid-derived suppressor cells (PMN-MDSC) inhibit immune responses in cancer, limit the effects of therapies and promote tumor cell metastasis. Here, we have identified a new precursor that differentiates into granulocytes in vitro and in vivo yet belong to the monocytic lineage. We have termed these cells monocyte-like precursors of granulocytes (MLPG). Under steady state conditions MLPG were absent in the spleen and barely detectable in the bone marrow (BM). In contrast, these cells significantly expanded in tumor-bearing mice. Selective depletion of monocytic cells had no effect on the number of granulocytes present in naïve mice but decreased the population of PMN-MDSC in tumor-bearing mice by 50%. The expansion of MLPG was found to be controlled by the down-regulation of the protein Rb1 and not the IRF8 transcription factor that is known to regulate the expansion of PMN-MDSC from classical granulocytes precursors. In cancer patients, putative MLPG were found within the population of CD15 CD14+HLA-DR-/lo M-MDSC. CXCR1+CD15 CD14+HLA-DR-/lo cells lacked immune suppressive activity but had potential to differentiate to neutrophils in contrast to monocytes and CXCR1- suppressive M-MDSC. These findings describe a mechanism of abnormal myelopoiesis in cancer and suggest potential new approaches for selective targeting of MDSC.
2019-05-30 | GSE131552 | GEO
Project description:Polymorphonuclear myeloid-derived suppressor cells (PMN-MDSC) inhibit immune responses in cancer, limit the effects of therapies and promote tumor cell metastasis. Here, we have identified a new precursor that differentiates into granulocytes in vitro and in vivo yet belong to the monocytic lineage. We have termed these cells monocyte-like precursors of granulocytes (MLPG). Under steady state conditions MLPG were absent in the spleen and barely detectable in the bone marrow (BM). In contrast, these cells significantly expanded in tumor-bearing mice. Selective depletion of monocytic cells had no effect on the number of granulocytes present in naïve mice but decreased the population of PMN-MDSC in tumor-bearing mice by 50%. The expansion of MLPG was found to be controlled by the down-regulation of the protein Rb1 and not the IRF8 transcription factor that is known to regulate the expansion of PMN-MDSC from classical granulocytes precursors. In cancer patients, putative MLPG were found within the population of CD15 CD14+HLA-DR-/lo M-MDSC. CXCR1+CD15 CD14+HLA-DR-/lo cells lacked immune suppressive activity but had potential to differentiate to neutrophils in contrast to monocytes and CXCR1- suppressive M-MDSC. These findings describe a mechanism of abnormal myelopoiesis in cancer and suggest potential new approaches for selective targeting of MDSC.
2019-05-30 | GSE131516 | GEO
Project description:Transcriptome comparsion of WT and CD300ld KO PMN-MDSC
| PRJNA820787 | ENA
Project description:A Toxoplasma gondii infection during pregnancy can result in spontaneous abortion, preterm labor, or congenital fetal defects. The decidual immune system plays a critical role in regulating the immune micro-environment and in the induction of immune tolerance. To better understand the factors that mediate the decidual immune response associated with the T. gondii infection, a large-scale study employing TMT proteomics was conducted to characterize the differential decidual immune proteomes from infected and uninfected human decidual immune cells samples. The decidual immune cells from 105 human voluntary abortion tissues were purified, and of the 5510 unique proteins identified, 181 proteins were found to be differentially abundant (>1.2-fold cutoff, P＜0.05) in the T. gondii-infected decidual immune cells. 11 proteins of 181 differentially expressed proteins associated with trophoblast invasion, placental development, intrauterine fetal growth, and immune tolerance were verified using a quantitative real-time polymerase chain reaction and western blotting. This systematic research identified a broad range of immune factors in human decidual immune cells, shedding a new insight into the decidual immune molecular mechanism for abnormal pregnancy outcomes associated with T. gondii infection.
2018-07-27 | PXD008448 | Pride
Project description:The pregnant decidua is infiltrated by many immune cells which are thought to originate in the bone marrow (BM) promoting pregnancy. In addition, BM-derived progenitor cells (BMDPCs) become non-hematopoietic endometrial cells. However, whether BMDPCs become non-immune decidual cells and their functional contribution to pregnancy were previously unknown. Here, we show that embryo implantation stimulates vast BMDPCs recruitment to decidua, where BMDPCs differentiate into non-hematopoietic stromal decidual cells. In addition, to determine the functional importance of BMDPCs to pregnancy, we used mice with endometrial stromal-specific defects precluding successful pregnancy. BM transplant (BMT) from wild-type (WT) into Hoxa11-/- mice, which lack decidualization, results in uterine transcriptional changes leading to stromal expansion, gland formation, and marked decidualization otherwise absent in Hoxa11-/- mice. By contrast, BMT from Hoxa11-/- into WT mice induces pregnancy loss. Importantly, in Hoxa11+/- mice, which have increased pregnancy losses, BMT from WT donors leads to normalized expression of numerous decidualization-related genes and rescue of pregnancy loss. Collectively, these findings reveal that BMDPCs have a novel non-hematopoietic physiologic contribution to decidual stroma, thereby playing indispensable roles in pregnancy establishment and maintenance.
2019-12-01 | GSE104842 | GEO