ArticleNature communications2022
Mouse fetal growth restriction through parental and fetal immune gene variation and intercellular communications cascade.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Article
- Partial embryo loss caused by disruption of the placental hormone CTRP6 coincides with dNK cell abnormalities during pregnancy.iScience · 2026Article
- Genetic admixture and adaptive signatures of Guanling cattle revealed by whole-genome sequence.BMC genomics · 2026Article
- Effects of the gut microbiota on placental angiogenesis and intrauterine growth in gnotobiotic mice.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Innate Lymphoid Cells in Reproductive Health and Disease.European journal of immunology · 2025Review
- The maternal-fetal interface at single-cell resolution: uncovering the cellular anatomy of the placenta and decidua.American journal of obstetrics and gynecology · 2025Review
- Extracellular vesicles as prospective biological indicators for midgestational placental complications in the mouse.Frontiers in cell and developmental biology · 2025Article
- A New Look at Immunogenetics of Pregnancy: Maternal Major Histocompatibility Complex Class I Educates Uterine Natural Killer Cells.International journal of molecular sciences · 2024Review
- Distribution-Agnostic Deep Learning Enables Accurate Single-Cell Data Recovery and Transcriptional Regulation Interpretation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Calorie restriction during gestation impacts maternal and offspring fecal microbiome in mice.Frontiers in endocrinology · 2024Article
- Biomarkers for Diagnosing and Treating Fetal Growth Restriction.Current medicinal chemistry · 2024Review
- Decidual macrophages and Hofbauer cells in fetal growth restriction.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
25 authors at 7 institutions in 4 countries.
Funding
Abstract
Fetal growth restriction (FGR) affects 5-10% of pregnancies, and can have serious consequences for both mother and child. Prevention and treatment are limited because FGR pathogenesis is poorly understood. Genetic studies implicate KIR and HLA genes in FGR, however, linkage disequilibrium, genetic influence from both parents, and challenges with investigating human pregnancies make the risk alleles and their functional effects difficult to map. Here, we demonstrate that the interaction between the maternal KIR2DL1, expressed on uterine natural killer (NK) cells, and the paternally inherited HLA-C*0501, expressed on fetal trophoblast cells, leads to FGR in a humanized mouse model. We show that the KIR2DL1 and C*0501 interaction leads to pathogenic uterine arterial remodeling and modulation of uterine NK cell function. This initial effect cascades to altered transcriptional expression and intercellular communication at the maternal-fetal interface. These findings provide mechanistic insight into specific FGR risk alleles, and provide avenues of prevention and treatment.
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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.