Project description:The first trimester is a critical window of maternal-fetal communication for pregnancy. RNA-sequencing of matched maternal decidua (4) and placenta (4) identified 91 sexually dimorphic receptor-ligand pairs across the maternal-fetal interface, 32 in females and 59 in males.
Project description:The subsets of immune cells within the human placenta are incompletely described. We used microarray to determine the transcriptional differences between two myeloid subsets in the term human placenta.
Project description:Maternal and fetal monocytes and tissue macrophages (decidual macrophages, Hofbauer cells) at the feto-maternal interface have different methylome.
Project description:Maternal and fetal monocytes and tissue macrophages (decidual macrophages, Hofbauer cells) at the feto-maternal interface have different methylome. Paired and balanced design. We compared maternal blood monocytes (MB) vs. cord blood monocytes (CB), maternal blood monocytes (MB) vs. decidual macrophages (Deci), cord blood monocytes (CB) vs placental macrophages (villi) and decidual macrophages (Deci) vs. placental macrophages (villi).
Project description:Immune tolerance at the maternal-fetal interface is required for fetal development. Excessive maternal interferon gamma (IFNγ) and interleukin-17 (IL-17) is linked to pregnancy complications, but the regulation of maternal IFNγ and IL-17 at the maternal-fetal interface (MFI) is poorly understood. Here we demonstrate a gut-placenta immune axis in pregnant mice in which the absence or perturbation of gut microbiota dysregulates maternal IFNγ and IL-17 responses at the MFI, resulting in fetal resorption. Microbiota-dependent tryptophan derivatives suppress IFNγ+ and IL-17+ T cells at the MFI by priming myeloid-derived suppressor cells (MDSCs) and gut-derived RORγt+ Tregs, respectively. The tryptophan derivative indole-3-carbinol, or tryptophan-metabolizing Lactobacillus murinus, rebalances the T cell response at the MFI and reduces fetal resorption in germ-free mice. Furthermore, MDSCs, RORγt+ Tregs, and microbiota-dependent tryptophan derivatives are dysregulated at the MFI in human recurrent miscarriage cases. Together, our findings identify microbiota-dependent immune tolerance mechanisms that promote fetal development.
Project description:The initiation of labor and preterm labor is a complex and precise physiological process involving a well-orchestrated dialogue between the mother and fetus. Immunological tolerance toward the semiallogeneic fetus is one of many maternal adaptations required for a successful pregnancy. T lymphocyte are major players of the adaptive immune system and balance tolerance and protection at the maternal-fetal interface. However, the dynamics, repertoire and subset programming of T cells across labor are still poorly understood. Here we integrated single-cell RNA sequencing and single-cell ATAC sequencing analyses of human decidua basalis and decidua parietalis from term and preterm labor to depict the composition of T cells at the maternal-fetal interface during late pregnancy and to investigate the potential mechanisms underlying the occurrence of preterm labor.