CCR8+ decidual regulatory T cells maintain maternal-fetal immune tolerance during early pregnancy
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1058460 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR27373700_1.fastq.gz | Fastqsanger.gz | |||
| SRR27373700_2.fastq.gz | Fastqsanger.gz | |||
| SRR27373701_1.fastq.gz | Fastqsanger.gz | |||
| SRR27373701_2.fastq.gz | Fastqsanger.gz |
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Project description:Regulatory T cells (Tregs) play crucial roles in maintaining maternal immune tolerance to the semi-allogeneic fetus during pregnancy, but Treg population heterogeneity and tissue-specific functions in human decidua remain largely unknown. Here, we conducted single-cell transcriptomic and T cell receptor sequencing of CD4+ T cells from first-trimester decidua and matched peripheral blood of pregnant women. These analyses identified a highly activated, immunosuppressive CCR8+ Treg subset specifically enriched in decidua (dTregs). CCR8+ dTregs are decreased in recurrent pregnancy loss (RPL) patients and abortion-prone model mice. Depletion of this subset with anti-CCR8 antibodies alters the decidual immune profile, increasing susceptibility to fetal loss. The CCR8 ligand, CCL1, is mainly produced by decidual CD49a+ NK cells and is also significantly decreased in RPL patients. By characterizing the landscape of dTregs in human early pregnancy, we identified CCR8+ dTregs as crucial for maintaining maternal-fetal tolerance, suggesting new potential strategies for RPL diagnosis and therapy.
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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.
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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.
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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.
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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.
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Project description:Toxoplasma gondii (T. gondii) is an obligate intracellular parasite that can lead to adverse pregnancy outcomes, particularly in early pregnancy. Previous studies have illustrated the landscape of decidual immune cells. However, the landscape of decidual immune cells in the maternal–fetal microenvironment during T. gondii infection remains unknown. In this study, we employed single-cell RNA sequencing to analyze the changes in human decidual immune cells following T. gondii infection. Our results showed that the proportion of 17 decidual immune cell clusters and the expression levels of 21 genes were changed after T. gondii infection. Differential gene analysis demonstrated that T. gondii infection induced the differential expression of 279, 312, and 380 genes in decidual NK, dMφ, and dT cells, respectively. Our findings first revealed that several previously unknown molecules in decidual immune cells changed following T. gondii infection. This result revealed that the function of maternal–fetal immune tolerance declined, whereas the killing ability of decidual immune cells enhanced, eventually contributing to the occurrence of adverse pregnancy outcomes. The results of this study provide a valuable resource for uncovering several novel molecules that play an important role in the occurrence of abnormal pregnancy outcomes induced by T. gondii infection.
2024-05-17 | GSE254302 | GEO
Project description:Bone marrow (BM)-derived progenitor cells (BMDPCs) are known to migrate and give rise to endometrial cells however their functional contribution to implantation and pregnancy are unknown . Here we show that implantation and pregnancy are strong stimuli for BMDPCs recruitment to the uterine decidua where BMDPCs differentiate into functional non-hematopoietic prolactin-producing decidual cells. Transcriptome analysis of implantation sites demonstrated that Hoxa11+/- mice transplanted with WT BM clustered hierarchically more closely with normal WT mice than with control Hoxa11+/- mice, showing normalized expression of numerous implantation-related genes. These findings reveal that BMDPCs have a major non-hematopoietic physiologic contribution to the decidual stroma, and thereby play an essential and previously unproven role in the establishment and maintenance of pregnancy.
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Project description:The transcriptional repressor Blimp-1/Prdm1 controls the maternal decidual response during pregnancy
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Project description:A successful pregnancy requires many physiological adaptations from the mother, including the establishment of tolerance towards the semiallogeneic fetus. Innate lymphoid cells (ILCs) have arisen as important players in immune regulation and tissue homeostasis at mucosal and barrier surfaces. Dimensionality reduction and transcriptomic analysis revealed the presence of two novel CD56Bright decidual ILCs, C10 and C2, that express divergent levels of Eomes. We found that decidual C10, C2, and cNKs correlated highly with previously identified first trimester decidual dNKs (dNK1-3). Functional analysis revealed polyfunctional profiles that depend on the nature of the stimulus, with a preference for IFNgamma and VEGF production. Overall, our data suggests persistence of pregnancy-specific decidual innate lymphocytes across pregnancy.
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Project description:Regulatory T (Treg) cells are essential for maternal immune tolerance of the fetus and placenta. In preeclampsia, aberrant Treg cell tolerance is implicated, but whether and how Treg cells affect the uterine vascular dysfunction thought to precede placental impairment and maternal vasculopathy is unclear. We utilized Foxp3 DTR mice to test the hypothesis that Treg cells are essential regulators of decidual spiral artery adaptation to pregnancy. Transient Treg cell depletion during early placental morphogenesis caused impaired remodeling of decidual spiral arteries and altered uterine artery function, resulting in late gestation fetal loss and fetal growth restriction. Treg cell depletion impaired acquisition of the activation receptor NKp46 on uterine natural killer (uNK cells) and was associated with reduced decidual synthesis of Treg cell-derived cytokines Il35, Il10 and Tgfb implicated in modulating uNK cell phenotype. When Treg cells were replaced, the adverse impact on uNK cell abundance and phenotype, decidual spiral artery remodeling, uterine artery function, and fetal loss was mitigated. These data implicate Treg cells as essential upstream drivers of uterine vascular adaptation to pregnancy through regulation of uNK cell recruitment and activation. The findings provide a mechanism linking impaired adaptive immune tolerance and altered spiral artery remodeling, two hallmark features of preeclampsia.
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