ReviewAnnals of translational medicine2022
Narrative review of the relationship between the maternal-fetal interface immune tolerance and the onset of preeclampsia.
Review in Annals of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Dynamic γδ T-cell Receptor remodeling and antigen-induced T-cell IFN-γ responses after SARS-CoV-2 infection during pregnancy: insights for γδ T-cell immunotherapy.Frontiers in immunology · 2026Article
- Bronchopulmonary dysplasia: signatures of monocyte-macrophage reactivity and tolerance define novel placenta-lung endotypes.Pediatric research · 2025Article
- COVID-19 vaccination and miscarriage risk: RNA-seq and bioinformatics analysis at the maternal-foetal interface.Journal of global health · 2025Article
- KCNK2-mediated regulation of MMP-2/9 by PlGF influences uterine artery function in pregnancy-induced hypertension.BMC pregnancy and childbirth · 2025Article
- Bidirectional Mendelian Randomization Analysis of Mood Disorders and Risk of Preeclampsia-Eclampsia.International journal of women's health · 2025Article
- Prediction and immune landscape study of potentially key autophagy-related biomarkers in preeclampsia with gestational diabetes mellitus.Frontiers in immunology · 2025Article
- Identification of genes involved in energy metabolism in preeclampsia and discovery of early biomarkers.Frontiers in immunology · 2025Article
- Identification of hub genes, diagnostic model, and immune infiltration in preeclampsia by integrated bioinformatics analysis and machine learning.BMC pregnancy and childbirth · 2024Article
- Macrophage Polarizations in the Placenta and Lung are Associated with Bronchopulmonary Dysplasia.bioRxiv : the preprint server for biology · 2024Article
- Palmitic Acid Upregulates CD96 Expression to Mediate Maternal-Foetal Interface Immune Tolerance by Inhibiting Cytotoxic Activity and Promoting Adhesion Function in Human Decidual Natural Killer Cells.Bioengineering (Basel, Switzerland) · 2023Article
- Single-cell profiling reveals immune disturbances landscape and HLA-F-mediated immune tolerance at the maternal-fetal interface in preeclampsia.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and Objective: The establishment of maternal-fetal interface immune tolerance is essential for successful pregnancy. Studies have shown that spontaneous abortion, recurrent abortion, and fetal growth restriction are related to maternal-fetal interface immune dysfunction. Preeclampsia is an idiopathic condition related to pregnancy which manifests as hypertension, proteinuria, and other target organ damage after 20 weeks of gestation. Although the etiology of preeclampsia is still unknown, its pathogenesis is thought to be related to genetics, environment, and metabolism. In recent years, more and more studies have been conducted on the mechanism of immune tolerance at the maternal-fetal interface and the relationship between immune dysregulation and the pathogenesis of preeclampsia. This paper summarizes the latest studies on this topic in order to find new insights into the pathogenesis of preeclampsia and make a reflection on clinical diagnosis and treatment in different phenotype of preeclampsia. Methods: The research and latest progress published from 2000 to December 2021 on the relationship between maternal-fetal interface immune tolerance and preeclampsia were broadly retrieved and researched using PubMed and Web of Science databases. Key Content and Findings: The mechanism of natural killer cells (NK cells) and macrophages at the maternal-fetal interface in immune tolerance, as well as their cytotoxicity and cytokine secretion dysfunction, may be related to the pathogenesis of preeclampsia. The expression of nonclassical type I human leukocyte antigen (HLA) on extravillous trophoblast (EVT) cell were down-regulated in decidua of preeclampsia, which may induce increase EVT death caused by activating of cytotoxic NK cell. In addition, genetic polymorphism of nonclassical type I HLA on the EVT cell membrane may be related to the pathogenesis of preeclampsia, although this is likely to be a combination of 3 nonclassical type I HLA genotypes and requires sequencing to verify. Conclusions: We demonstrated how the maternal-fetal interface immune dysfunction contribute to the pathogenesis of preeclampsia, further study and clinical trial based on this theory of pathogenesis may reveal new immune treatment method of preeclampsia.
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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.