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Metabolic reprogramming driven by impaired trophoblasts and decidual XCR1+PMN-MDSCs crosstalk controls adverse outcomes in advanced maternal age

ABSTRACT: Decidual polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) are crucial for maternal–fetal stability and accumulate to support fetal development. Although advanced maternal age (AMA) increases the risk of adverse outcomes, the regulatory role and mechanism of decidual PMN-MDSCs in these outcomes remain unclear. Herein, the XCL1–XCR1 interaction mediated specific crosstalk between trophoblast cells and decidual PMN-MDSCs in both humans and mice. Single-cell sequencing identified a decidual PMN-MDSCs subset highly expressing XCR1 markedly reduced in AMA. Impaired XCL1-stimulated decidual XCR1+PMN-MDSCs delayed fetal growth in AMA and Xcr1-/- pregnant mice. Perinatal XCL1 supplementation and oltipraz treatment rescued these functions by activating decidual XCR1+PMN-MDSCs in AMA mice, not Xcr1-/- pregnant mice. The XCL1–XCR1 axis induced FOXO1 nuclear localization, regulating oxidative phosphorylation-related targets and enabling metabolic processes. Hence, XCL1–XCR1 crosstalk between trophoblast cells and PMN-MDSCs is critical in driving metabolic reprogramming of decidual XCR1+PMN-MDSCs and controlling adverse outcomes caused by AMA.

ORGANISM(S): Homo sapiens

PROVIDER: GSE289975 | GEO | 2026/04/08

REPOSITORIES: GEO

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Metabolic reprogramming driven by impaired trophoblasts and decidual XCR1+PMN-MDSCs crosstalk controls adverse outcomes in advanced maternal age [CUT&Tag]

Project description:Decidual polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) are crucial for maternal–fetal stability and accumulate to support fetal development. Although advanced maternal age (AMA) increases the risk of adverse outcomes, the regulatory role and mechanism of decidual PMN-MDSCs in these outcomes remain unclear. Herein, the XCL1–XCR1 interaction mediated specific crosstalk between trophoblast cells and decidual PMN-MDSCs in both humans and mice. Single-cell sequencing identified a decidual PMN-MDSCs subset highly expressing XCR1 markedly reduced in AMA. Impaired XCL1-stimulated decidual XCR1+PMN-MDSCs delayed fetal growth in AMA and Xcr1-/- pregnant mice. Perinatal XCL1 supplementation and oltipraz treatment rescued these functions by activating decidual XCR1+PMN-MDSCs in AMA mice, not Xcr1-/- pregnant mice. The XCL1–XCR1 axis induced FOXO1 nuclear localization, regulating oxidative phosphorylation-related targets and enabling metabolic processes. Hence, XCL1–XCR1 crosstalk between trophoblast cells and PMN-MDSCs is critical in driving metabolic reprogramming of decidual XCR1+PMN-MDSCs and controlling adverse outcomes caused by AMA.

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Metabolic reprogramming driven by impaired trophoblasts and decidual XCR1+PMN-MDSCs crosstalk controls adverse outcomes in advanced maternal age [RNA-Seq]

2026-04-08 | GSE288396 | GEO

Whole genome expression profile of human decidual PMN-MDSC and autologous neutrophils in normal pregnancy

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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Next Generation Sequencing of human circulating neutrophils treated with decidual explant supernatant or not

Project description:Decidual microenvironment can induce circulating neutrophils to acquire the phenotypes and functions of decidual polymorphonuclear myeloid-derived suppressor cell (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 neutrophils treated with decidual explant supernatant (DES) or not (n=3). Total RNA were extracted. Transcriptome libraries were generated with the Illumina TruseqTM RNA sample prep Kit, and sequencing was performed on the Illumina Novaseq 6000 platform. There were differences of gene expression after DES treatment.

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Proteomic profiling of human decidual immune proteins during Toxoplasma gondii infection

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

Whole genome expression profile of human decidual PMN-MDSC in normal pregnancy and unexplained recurrent pregnancy loss

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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Comparision of transcriptomes between murine WT type 1 conventional DCs to XCR1-deficient type 1 conventional DCs

Project description:We sought to compare the overall transcriptomic differences between TLR stimulated WT and XCR1-deficient type 1 conventional DCs. In addition, we also wanted to investigate functional role of XCR1 signaling in WT type 1 conventional DCs by treating recombinant murine XCL1, a ligand of XCR1 to these cells as well

2023-06-01 | GSE228392 | GEO

The XCL1-XCR1 axis supports intestinal tissue residency and anti-tumor immunity

Project description:Tissue-resident memory T cells (TRM) provide frontline protection against pathogens and emerging malignancies. Tumor-infiltrating lymphocytes (TIL) with TRM features are associated with improved clinical outcomes. However, the cellular interactions that program TRM differentiation and function are not well understood. Using murine genetic models and targeted spatial transcriptomics, we found that the CD8+ T cell-derived chemokine XCL1 is critical for TRM formation and conventional DC1 (cDC1) support the positioning of intestinal CD8+ T cells during acute viral infection. In tumors, enforced Xcl1 expression by antigen-specific CD8+ T cells promoted intratumoral cDC1 accumulation and T cell persistence, leading to improved overall survival. Notably, analysis of human TIL and TRM revealed conserved expression of XCL1 and XCL2. Thus, we have shown that the XCL1-XCR1 axis plays a non-cell autonomous role in guiding intestinal CD8+ TRM spatial differentiation and tumor control.

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Xcr1+ type 1 conventional dendritic cells are essential mediators for atherosclerosis progression

Project description:Atherosclerosis is characterized by lipid accumulation within plaques, leading to foam cell formation and inflammatory response within the aortic lesions. Lipid disorders have been extensively investigated, however the cellular and molecular mechanisms that trigger the inflammatory response in atherosclerotic plaques remain far from being fully understood. Xcr1+ cDC1 cells are newly identified antigen-presenting cells in activating immune cells. However, the role of cDC1 cells in atherosclerosis development remains highly controversial. We first confirmed the presence of cDC1 within human atherosclerotic plaques and discovered a significant association between the increasing cDC1 numbers and atherosclerosis progression in mice. Subsequently, we established Xcr1Cre-Gfp Rosa26LSL-DTA Apoe–/– mice, a novel and complex genetic model, in which cDC1 was constitutively depleted in vivo during atherosclerosis development. Intriguingly, we observed a notable reduction in atherosclerotic lesions in hyperlipidemic mice, alongside suppressed T cell activation of both CD4+ and CD8+ subsets in the aortic plaques. Notably, aortic macrophages and serum lipid levels were not significantly changed in the cDC1-depleted mice. Single-cell RNA sequencing revealed heterogeneity of Xcr1+ cDC1 cells across the aorta and lymphoid organs under hyperlipidemic conditions. As Xcr1 is the sole receptor for Xcl1, we next explored to target Xcr1+ cDC1 cells via Xcl1 by establishing Xcl1–/–Apoe–/– mice. Xcl1–/–Apoe–/– mice exhibited decreased atherosclerotic plaque formation and reduced aortic cDC1 accumulation, indicating that Xcl1 contributes to cDC1-mediated atherosclerotic lesion development. Our results reveal crucial roles of cDC1 in atherosclerosis progression and provide insights into the development of immunotherapies by targeting cDC1 through Xcl1.

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Single-cell transcriptome analyses reveal disturbed decidual microenvironment in women of advanced maternal age

Project description:Background: Advanced maternal age (AMA) increases pregnancy risk. However, uterine-specific mechanisms independent of oocyte and embryo quality remain poorly defined. This study aimed to characterise the decidual microenvironment in women of AMA to identify key pathological changes and regulatory pathways. Methods and Results: Through integrated histology, organoid modelling, and high-resolution scRNA-seq of first-trimester decidua from women of AMA and controlled reproductive age, we uncovered a pathologically remodelled decidual microenvironment characterised by fibroblast expansion, immune depletion, and disrupted intercellular communication in the AMA decidua. Central to this pathology was hyperactivated TGF-β signalling, driving fibroblast-to-myofibroblast transition (FMT) and extracellular matrix overproduction, thereby fuelling fibrosis. Aberrant TGF-β further impaired decidual stromal cell (DSC) differentiation, causing failure of the essential mesenchymal-to-epithelial transition (EMT). We identified PRR15 as a novel DSC-specific regulator that is markedly suppressed in AMA. PRR15 deficiency unleashed hyperactive TGF-β/SMAD signalling, directly causing decidualization failure, enhanced fibrosis, and aborted DSC differentiation. Epithelial-mesenchymal transition and immune cell reprogramming towards profibrotic phenotypes further amplify the fibrotic pathology. Conclusion: This study established the aged decidual microenvironment, orchestrated by dysregulated TGF-β signalling and PRR15 loss, as a critical independent determinant of reproductive failure in AMA. Thus, it unveils novel diagnostic and therapeutic targets and strategies.

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