ArticleCellular & molecular immunology2016
An imbalance between innate and adaptive immune cells at the maternal-fetal interface occurs prior to endotoxin-induced preterm birth.
Article in Cellular & molecular immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 76 citations in OpenAlex.
- Fetal T Cell Activation in the Amniotic Cavity during Preterm Labor: A Potential Mechanism for a Subset of Idiopathic Preterm Birth.Journal of immunology (Baltimore, Md. : 1950) · 2019Trial
- Effector and Activated T Cells Induce Preterm Labor and Birth That Is Prevented by Treatment with Progesterone.Journal of immunology (Baltimore, Md. : 1950) · 2019Trial
- The Cellular Transcriptome in the Maternal Circulation During Normal Pregnancy: A Longitudinal Study.Frontiers in immunology · 2019Trial
- The altered PD-1/PD-L1 pathway delivers the 'one-two punch' effects to promote the Treg/Th17 imbalance in pre-eclampsia.Cellular & molecular immunology · 2018Trial
- Maternal Microbiome in Fetal Programming: A One Health Perspective on Translational Implications for Early-Life Health.Microorganisms · 2026Review
- Heterogeneity in inflammatory responses to endotoxin at the fetomaternal interface.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Exosomal delivery of IL-10: Biodistribution, pharmacokinetics, and preterm birth prevention strategies.Extracellular vesicle · 2025Article
- The maternal-fetal interface at single-cell resolution: uncovering the cellular anatomy of the placenta and decidua.American journal of obstetrics and gynecology · 2025Review
- The landscape of decidual immune cells at the maternal-fetal interface in parturition and preterm birth.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Th17/Treg Cell Imbalance May Contribute to Spontaneous Preterm Labor.Journal of immunology research · 2025Review
- Extracellular Vesicles-mediated recombinant IL-10 protects against ascending infection-associated preterm birth by reducing fetal inflammatory response.Frontiers in immunology · 2023Article
- Association between Pet Ownership and Threatened Abortion in Pregnant Women: The China Birth Cohort Study.International journal of environmental research and public health · 2022Article
- Gestationally dependent immune organization at the maternal-fetal interface.Cell reports · 2022Article
- The immunobiology of preterm labor and birth: intra-amniotic inflammation or breakdown of maternal-fetal homeostasis.Reproduction (Cambridge, England) · 2022Review
- IL-22 Plays a Dual Role in the Amniotic Cavity: Tissue Injury and Host Defense against Microbes in Preterm Labor.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Differences in cord blood extracellular vesicle cargo in preterm and term births.American journal of reproductive immunology (New York, N.Y. : 1989) · 2022Article
- CCL2: An important cytokine in normal and pathological pregnancies: A review.Frontiers in immunology · 2022Review
- Sexually Dimorphic Crosstalk at the Maternal-Fetal Interface.The Journal of clinical endocrinology and metabolism · 2020Article
- Pregnancy-specific transcriptional changes upon endotoxin exposure in mice.Journal of perinatal medicine · 2020Article
- Novel pathways of inflammation in human fetal membranes associated with preterm birth and preterm pre-labor rupture of the membranes.Seminars in immunopathology · 2020Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Preterm birth (PTB) is the leading cause of neonatal morbidity and mortality worldwide. A transition from an anti-inflammatory state to a pro-inflammatory state in the mother and at the maternal-fetal interface has been implicated in the pathophysiology of microbial-induced preterm labor. However, it is unclear which immune cells mediate this transition. We hypothesized that an imbalance between innate and adaptive immune cells at the maternal-fetal interface will occur prior to microbial-induced preterm labor. Using an established murine model of endotoxin-induced PTB, our results demonstrate that prior to delivery there is a reduction of CD4+ regulatory T cells (Tregs) in the uterine tissues. This reduction is neither linked to a diminished number of Tregs in the spleen, nor to an impaired production of IL10, CCL17, or CCL22 by the uterine tissues. Endotoxin administration to pregnant mice does not alter effector CD4+ T cells at the maternal-fetal interface. However, it causes an imbalance between Tregs (CD4+ and CD8+), effector CD8+ T cells, and Th17 cells in the spleen. In addition, endotoxin administration to pregnant mice leads to an excessive production of CCL2, CCL3, CCL17, and CCL22 by the uterine tissues as well as abundant neutrophils. This imbalance in the uterine microenvironment is accompanied by scarce APC-like cells such as macrophages and MHC II+ neutrophils. Collectively, these results demonstrate that endotoxin administration to pregnant mice causes an imbalance between innate and adaptive immune cells at the maternal-fetal interface.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.