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Regulatory T Cells Play a Central Role in a Subset of Idiopathic Preterm Birth and Adverse Neonatal Outcomes

ABSTRACT: Regulatory T Cells Play a Central Role in a Subset of Idiopathic Preterm Birth and Adverse Neonatal Outcomes

PROVIDER: PRJNA606812 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11091570.fastq.gz	Fastqsanger.gz
	SRR11091571.fastq.gz	Fastqsanger.gz
	SRR11091572.fastq.gz	Fastqsanger.gz
	SRR11091573.fastq.gz	Fastqsanger.gz
	SRR11091574.fastq.gz	Fastqsanger.gz

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Regulatory T Cells Play a Central Role in a Subset of Idiopathic Preterm Birth and Adverse Neonatal Outcomes

Project description:Regulatory T cells (Tregs) have been exhaustively investigated during early pregnancy; however, their role later in gestation is poorly understood. Herein, we report that functional Tregs are reduced at the maternal-fetal interface in a subset of women with idiopathic preterm labor/birth (PTB), which is accompanied by a concomitant increase in Tc17 cells. In mice, depletion of functional Tregs during late gestation induced PTB and adverse neonatal outcomes, which were rescued by the adoptive transfer of such cells. Treg depletion did not alter obstetrical parameters in the mother; yet, it increased susceptibility to endotoxin-induced PTB. The mechanisms whereby the loss of Tregs induces adverse perinatal outcomes involved tissue-specific immune responses and mild systemic maternal inflammation together with dysregulation of developmental and cellular processes in the placenta, in the absence of intra-amniotic inflammation. These findings provide mechanistic evidence supporting a central role for Tregs in the pathophysiology of idiopathic PTB and adverse neonatal outcomes.

2020-06-04 | GSE145357 | GEO

Assessing placental maturity through histological and transcriptomic analyses in idiopathic spontaneous preterm birth

Project description:Assessing placental maturity through histological and transcriptomic analyses in idiopathic spontaneous preterm birth

2019-12-25 | GSE118442 | GEO

Regulatory T Cells Play a Role in a Subset of Idiopathic Preterm Labor/Birth and Adverse Neonatal Outcomes.

Project description:Regulatory T cells (Tregs) have been exhaustively investigated during early pregnancy; however, their role later in gestation is poorly understood. Herein, we report that functional Tregs are reduced at the maternal-fetal interface in a subset of women with idiopathic preterm labor/birth, which is accompanied by a concomitant increase in Tc17 cells. In mice, depletion of functional Tregs during late gestation induces preterm birth and adverse neonatal outcomes, which are rescued by the adoptive transfer of such cells. Treg depletion does not alter obstetrical parameters in the mother, yet it increases susceptibility to endotoxin-induced preterm birth. The mechanisms whereby depletion of Tregs induces adverse perinatal outcomes involve tissue-specific immune responses and mild systemic maternal inflammation, together with dysregulation of developmental and cellular processes in the placenta, in the absence of intra-amniotic inflammation. These findings provide mechanistic evidence supporting a role for Tregs in the pathophysiology of idiopathic preterm labor/birth and adverse neonatal outcomes.

| S-EPMC7396155 | biostudies-literature

Preterm birth CVF proteomics discovery

Project description:Preterm birth, defined as birth <37 weeks of gestation, is a leading cause of infant morbidity and mortality. In the United States, approximately 12% of all births are preterm.1 Despite decades of research, there has been little progress in developing effective interventions to prevent preterm birth. In fact, the rate of preterm birth has increased slightly over the last several decades.2 The ultimate goal of the Genomic and Proteomic Network for Preterm Birth Research (GPN-PBR) is to identify possible biomarkers that could predict the susceptibility to spontaneous preterm birth (SPTB) as well as to shed light on the molecular mechanisms involved in its etiologies. Understanding those mechanisms will help us predict SPTB and may facilitate the introduction of more effective prevention and treatment strategies.

2014-08-28 | PXD001268 | Pride

Assessing placental maturity through histological and transcriptomic analyses in idiopathic spontaneous preterm birth

Project description:Assessing placental maturity through histological and transcriptomic analyses in idiopathic spontaneous preterm birth

| PRJNA485683 | ENA

Biochemistry of spontaneous preterm birth

Project description:Biochemistry of spontaneous preterm birth

| PRJNA493125 | ENA

CIDR Preterm Birth Boston Cohort

Project description:CIDR Preterm Birth Boston Cohort

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miRNA-Seq of human placenta: spontaneous preterm birth in the presence of intra-amniotic infection/inflammation and controls

2016-06-14 | GSE73713 | GEO

RNA-Seq of human placenta: spontaneous preterm birth in the presence of intra-amniotic infection/inflammation and controls

2016-06-14 | GSE73712 | GEO

miRNA-Seq of human placenta: spontaneous preterm birth in the presence of intra-amniotic infection/inflammation and controls

Project description:Using RNA-sequencing (RNA-Seq and miRNA-Seq), we analyzed paired villous trophoblast and decidual basalis transcriptomes of 15 women pregnant with singleton gestations grouped as follows: (1) spontaneous preterm birth (PTB) in the setting of amniocentesis-proven intra-amniotic infection (IAI) and histological chorioamnionits (n=5; GA median [range]: 26 [25-31] weeks); (2) spontaneous idiopathic preterm birth (iPTB, n=5, GA: 32 [30-33] weeks); and (3) term normal pregnancy, that delivered a heathy infant by cesarean section in the absence of labor (n=5; GA: 39 [38-39] weeks). The primary goal of this study was to identify differentially expressed transcripts and illuminate molecular mechanisms distinguishing IAI-associated PTBs from spontaneous PTBs in the absence of IAI. We further compared iPTB specimens to term specimens to determine genes differentially regulated with advancing gestational age and following spontaneous PTB without IAI. Finally, we determined transcripts selectively expressed in either the villous trophoblast or decidua basalis in each clinical context. Raw data for this series are not available because consent forms do not allow for public access to raw data.

2016-06-14 | E-GEOD-73713 | biostudies-arrayexpress

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