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Regulatory T cells in human pregnancy

ABSTRACT: Transplacental immune programming refers to the concept that during pregnancy, significant crosstalk occurs between the maternal and fetal immune system, with consequent long‐term effects especially for the offspring. In this study, we searched for evidence of transplacental programming in cellular immunity. We made the surprising observation that there is a stringent and specific correlation of regulatory T cells (Treg) between the mother and the fetus. Gene microarray analysis indicates that interleukin 10 (IL‐10) might be involved in transplacental Treg alignment. This is further supported by the direct correlation of IL‐10 at a protein level between maternal fetal dyads. In vitro data provide evidence that IL‐10 may regulate the homeostatic balance between Tregs and non‐Tregs through selective upregulation of the anti‐apoptotic molecule Bcl‐2 in Tregs. Induction of IL‐10 might be triggered by fetus‐derived estriol (E3), which readily crosses the placenta and correlates with maternal IL‐ 10 levels. Our study represents the first example of transplacental regulation of cellular immunity between the mother and the fetus. These novel findings might have major implications for pregnancy related‐changes in the maternal and fetal immune system, and provide possible mechanistic insights into how prenatal influences can lead to subsequent immunopathologies, such as allergy and autoimmunity.

ORGANISM(S): Homo sapiens

PROVIDER: GSE31976 | GEO | 2013/11/04

SECONDARY ACCESSION(S): PRJNA144971

REPOSITORIES: GEO

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regulatory T cells in human pregnancy

Project description:Transplacental immune programming refers to the concept that during pregnancy, significant crosstalk occurs between the maternal and fetal immune system, with consequent long‐term effects especially for the offspring. In this study, we searched for evidence of transplacental programming in cellular immunity. We made the surprising observation that there is a stringent and specific correlation of regulatory T cells (Treg) between the mother and the fetus. Gene microarray analysis indicates that interleukin 10 (IL‐10) might be involved in transplacental Treg alignment. This is further supported by the direct correlation of IL‐10 at a protein level between maternal fetal dyads. In vitro data provide evidence that IL‐10 may regulate the homeostatic balance between Tregs and non‐Tregs through selective upregulation of the anti‐apoptotic molecule Bcl‐2 in Tregs. Induction of IL‐10 might be triggered by fetus‐derived estriol (E3), which readily crosses the placenta and correlates with maternal IL‐ 10 levels. Our study represents the first example of transplacental regulation of cellular immunity between the mother and the fetus. These novel findings might have major implications for pregnancy related‐changes in the maternal and fetal immune system, and provide possible mechanistic insights into how prenatal influences can lead to subsequent immunopathologies, such as allergy and autoimmunity. T-reg and non-Treg samples of non pregnant women, and matched cord blood and maternal blood T-regs and non-T-regs

2013-11-04 | E-GEOD-31976 | biostudies-arrayexpress

Fetal blood transcriptome in maternal anti-fetal rejection

Project description:Both the fetus and the mother who are involved in maternal anti-fetal rejection during pregnancy show distinct alterations in the peripheral blood transcriptome Total RNA isolated from umbilical cord blood and maternal blood was compared between cases without (Normal) and with maternal anti-fetal rejection (FIRS2) using whole genome DASL assay.

2012-03-31 | E-GEOD-28387 | biostudies-arrayexpress

Fetal blood transcriptome in maternal anti-fetal rejection

Project description:Both the fetus and the mother who are involved in maternal anti-fetal rejection during pregnancy show distinct alterations in the peripheral blood transcriptome

2012-04-01 | GSE28387 | GEO

Maternal antioxidant treatment prevents the adverse effects of prenatal stress on the offspring's brain and behavior [NanoString nCounter rat miRNA]

Project description:Maternal exposure to stress during pregnancy is associated with an increased risk of psychiatric disorders in the offspring in later life. The mechanisms through which the effects of maternal stress are transmitted to the fetus are unclear, however the placenta, as the interface between mother and fetus, is likely to play a key role. Using a rat model, we investigated a role for placental oxidative stress in conveying the effects of maternal social stress to the fetus and the potential for treatment using a nanoparticle-bound antioxidant to prevent adverse outcomes in the offspring. Maternal psychosocial stress increased circulating corticosterone in the mother, but not in the fetuses. Maternal stress also induced oxidative stress in the placenta, but not in the fetal brain. Blocking oxidative stress using an antioxidant prevented the prenatal stress-induced anxiety phenotype in the male offspring, and prevented sex-specific neurobiological changes, specifically a reduction in dendrite lengths in the hippocampus, as well as reductions in the number of parvalbumin-positive neurons and GABA receptor subunits in the hippocampus and basolateral amygdala of the male offspring. Importantly, many of these effects were mimicked in neuronal cultures by application of placental-conditioned medium or fetal plasma from stressed pregnancies, indicating molecules released from the placenta may mediate the effects of prenatal stress on the fetal brain. Indeed, both placenta-conditioned medium and fetal plasma contained differentially abundant microRNAs following maternal stress, and their predicted targets were enriched for genes relevant to nervous system development and psychiatric disorders. The results highlight placental oxidative stress as a key mediator in transmitting the maternal social stress effects on the offspring's brain and behaviour, and offer a potential intervention to prevent stress-induced fetal programming of affective disorders.

2020-12-01 | GSE130573 | GEO

Regulation of fetal liver transcription by maternal nutritional stress

Project description:Pregnancy is a time of extreme metabolic demand that requires coordinated adaptations between mother and fetus. To determine the contributions of maternal and fetal metabolism to metabolic plasticity during gestation, mice with a liver-specific Carnitine Palmitoyltransferase-2 knockout mice (Cpt2-/-), or Pparα KO mice were subjected to late-gestation nutrient stress, a 24hr fast from E16.5 to E17.5. The fetal response to maternal fasting was dominated by maternal lipid metabolism as the loss of maternal hepatic fatty acid oxidation or Pparα signaling accelerated fetal liver transcriptional programing. These data show that maternal nutritional environment is a major driver of perinatal metabolic programing and plasticity.

2019-09-20 | GSE129368 | GEO

Seeking Gene Candidates Responsible for Developmental Origins of Health and Disease (DOHaD)

Project description:Human epidemiological evidence has led scientists to theorize that undernutrition during gestation is an important early origin of adult diseases. Animal models have successfully demonstrated that maternal diet could contribute to some of adult diseases. Undernutrition is perceived harmful in pregnant women whereas calorie restriction is a strategy proven to extend healthy and maximum life span in adult. This diagrammatically opposite effect of nutritional condition might provide us hints to search for genes underlying health conditions. Here, we have initiated a study examining the effect of undernutrition on maternal and fetal livers, utilizing high-throughput DNA microarray analysis for screening genome-wide changes in their transcriptomes. Briefly, pregnant mice were exposed to food deprivation (FD) on gestation day (GD) 17, and caesarean section was performed on GD18. Control mice were supplied with chow ad libitum till sacrifice. Total RNA extracted from mother and fetal livers for each control and treatment (FD) was analyzed with an Agilent mouse whole genome DNA chip. Total of 3058 and 3126 up (>1.5 fold)- and down (<0.75 fold)-regulated genes, and 1475 and 1225 up- (>1.5 fold)- and down (<0.75 fold)-regulated genes showed differential expression at the mRNA level, in the maternal and fetal livers, respectively. Interestingly, 103 genes up-regulated in mother were down-regulated in fetus, whereas 108 down-regulated maternal genes were up-regulated in fetus; these 211 genes are potential candidates related to longevity or health. The role of some of these genes, in context of the proposed mechanisms for developmental origins of health and disease is discussed. Comparison between mouse control and FD livers in fetus and mother was performed. Five to ten biological replicates were used, and pooled total RNA from each condition (control and FD) was dye-swaped.

2011-04-01 | E-GEOD-28175 | biostudies-arrayexpress

Fetal liver programming induced by placental endocrine malfunction

Project description:The placenta acts as an interface between the mother and fetus, regulating nutrient transport and secreting hormones which impact maternal metabolism. Complications during pregnancy, such as placental endocrine malfunction, programme offspring to develop metabolic disease during adulthood, in part via changes in gene expression in critical metabolic organs, such as the liver, during fetal development. Placental endocrine malfunction was induced via the misexpression of two imprinted genes (Igf2 and H19) exclusively in the endocrine zone of the mouse placenta, to study the consequences this has on fetal hepatic gene expression.

2023-11-30 | E-MTAB-11457 | biostudies-arrayexpress

Maternal IL-10 restricts fetal emergency myelopoiesis [scATAC-seq]

Project description:We investigated how late fetal liver (FL) mouse hematopoieitic stem and progenitor cells (HSPC) respond to inflammation, with the hypothesis that deficits in engagement of emergency myelopoiesis (EM) pathways could limit neutrophil output and contribute to perinatal neutropenia, ultimately explaining the susceptibility of neonates to inflammation and infection. We show that fetal HSPCs are biased toward erythroid and lymphoid cell production at steady state and fail to mount classical EM responses in vivo. Despite being capable of responding to EM-inducing stimuli in vitro, we find that maternal factors like interleukin-10 (IL-10) restrict fetal HSPCs from activating EM pathways in utero. Accordingly, we find that loss of maternal IL-10 restores EM activation in fetal HSPCs but at a cost of premature parturition. These results reveal the evolutionary trade-off inherent in maternal anti-inflammatory responses that maintain pregnancy but render the fetus susceptible to infection.

2024-02-29 | GSE240914 | GEO

Maternal IL-10 restricts fetal emergency myelopoiesis [scRNA-seq]

2024-02-29 | GSE240913 | GEO

Maternal IL-10 restricts fetal emergency myelopoiesis [Bulk RNA-seq]

2024-02-29 | GSE240912 | GEO