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SOX4 Mediated Differentiation of Specific T Lymphocyte Subsets at the Maternal-Fetal Interface Contributes to Preterm Labor [RNA-Seq]

ABSTRACT: Preterm labor is one of the most common pregnancy complications and the leading cause of perinatal neonatal mortality, and its prevention and treatment strongly rely on the depiction of mechanisms underlying the initiation of labor. T lymphocyte are major players of the adaptive immune system and balance tolerance and protection at the maternal-fetal interface. 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. Our research identified CD8-naïve-SOX4 subset associated with preterm labor, which showed a significant decrease of proportion in the basalis decidua of preterm labor. The transcription factor SOX4 was specifically expressed in naïve CD8+ T cells and was significantly downregulated in the CD8-naïve-SOX4 subset in the decidua basalis of preterm labor. Mechanically, SOX4 plays a pivotal role in mediating T cell differentiation and promotes the differentiation of naïve CD8+ T cells into effector CD8+ T cells in the preterm labor based on pseudotime analysis. We generated a co-culture system to simulate cellular interactions between T cells and uterine smooth muscle cells or amniotic epithelial cells at the maternal-fetal interface, and RNA-sequencing analysis of myometrial cells and amniotic epithelial cells co-cultured with SOX4-deficient T cells revealed disruption of actin filament assembly in uterine smooth muscle cells and F-actin rearrangement in amniotic epithelial cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE298146 | GEO | 2026/05/13

REPOSITORIES: GEO

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Project description:Preterm birth is a main determinant of neonatal mortality and morbidity and a major contributor to the overall mortality and burden of disease. However, precise phenotyping of the preterm birth is hampered by the imprecise definition of the clinical phenotype and complexity of the molecular phenotype due to multiple pregnancy tissue types and molecular processes that may contribute to the preterm birth. The studyâ??s aim was to comprehensively evaluate the mRNA transcriptome that characterizes preterm and term labor using precisely phenotyped samples. Expression profiles of 73 genes and non-coding RNA sequences uniquely identified the four groups of patients: delivering preterm with (PL) and without labor (PNL), term with (TL) and without labor (TNL). The largest differences in gene expression among the four groups occurred in decidua, chorion and amnion. The gene expression profiles showed suppression of chemokines expression in TNL, withdrawal of this suppression in TL, activation of multiple pathways of inflammation in PL, and an immune rejection profile in PNL. The genes constituting expression signatures showed over-representation of three putative regulatory elements in their 5â?? and 3â??UTR regions. The results suggest that pregnancy is maintained by downregulation of chemokines at the maternal-fetal interface. Withdrawal of this downregulation results in the term birth and its overriding by the activation of multiple pathways of the immune system in the preterm birth. Complications of the pregnancy associated with impairment of placental function, which necessitated premature delivery of the fetus in the absence of labor, show gene expression patterns associated with immune rejection. 183 total RNA samples from 8 tissue types collected from 35 women grouped into six categories of pregnancy outcome. One microarray replicate per sample. Other Contributors: Radek Bukowski, Sam Parry and the NICHD Genomic and Proteomic Network for Preterm Birth Research

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SOX4 Mediated Differentiation of Specific T Lymphocyte Subsets at the Maternal-Fetal Interface Contributes to Preterm Labor [RNA-Seq]

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