ArticleNature communications2017
Activated NK cells cause placental dysfunction and miscarriages in fetal alloimmune thrombocytopenia.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 111 citations in OpenAlex.
- Toxoplasma gondii infection reduces CD59 expression through downregulation of JAK2/STAT3 signaling axis to enhance decidual NK cell cytotoxicity via the RAS/MAPK pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- New perspectives on fetal and neonatal alloimmune thrombocytopenia for obstetricians.Frontiers in immunology · 2026Review
- The Immunology of Transfusion Medicine: Past, Present, and Future.Methods in molecular biology (Clifton, N.J.) · 2026Review
- Single-cell RNA sequencing of leukocytes at the maternal-fetal interface in physiological and pathological Nodal-deficient pregnancies.Frontiers in immunology · 2026Article
- Maternal Diet-Induced Excess Adiposity in Mice Disrupts Mid-Gestation Decidual Immune and Vascular Homeostasis Without Impairing Spiral Artery Remodeling.Acta physiologica (Oxford, England) · 2025Article
- Dual Role of Natural Killer Cells in Early Pregnancy: Immunopathological Implications and Therapeutic Potential in Recurrent Spontaneous Abortion and Recurrent Implantation Failure.Cell proliferation · 2025Review
- Maternal and placental galectins: key players in the feto-maternal symbiotic tango.Seminars in immunopathology · 2025Review
- Enrichment of decidual CD11c + CD8 + T cells with altered immune function in early pregnancy loss.Nature communications · 2025Article
- Flow cytometric analysis of the murine placenta to evaluate nanoparticle platforms during pregnancy.Placenta · 2025Article
- Targeting Decidual CD16Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- 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
- B Cell Responses to the Placenta and Fetus.Annual review of pathology · 2025Review
- Development of a humanized mouse model with functional human materno-fetal interface immunity.JCI insight · 2024Article
- Association of recurrent implantation failure and recurrent pregnancy loss with peripheral blood natural killer cells and interferon-gamma level.Obstetrics & gynecology science · 2024Article
- IL-21R-STAT3 signalling initiates a differentiation program in uterine tissue-resident NK cells to support pregnancy.Nature communications · 2023Article
- Omega-3 fatty acid supplements and recurrent miscarriage: A perspective on potential mechanisms and clinical evidence.Food science & nutrition · 2023Review
- Review
- Analysis of FCGR3A-p.176Val variants in women with recurrent pregnancy loss and the association with CD16a expression and anti-HLA antibody status.Scientific reports · 2023Article
- Foetal Intrapartum Compromise at Term: Could COVID-19 Infection Be Involved? A Case Report.Medicina (Kaunas, Lithuania) · 2023Article
- B2 cells contribute to hypertension and natural killer cell activation possibly via AT1-AA in response to placental ischemia.American journal of physiology. Renal physiology · 2023Article
Corrections and comments
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Authors and funding
22 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Miscarriage and intrauterine growth restriction (IUGR) are devastating complications in fetal/neonatal alloimmune thrombocytopenia (FNAIT). We previously reported the mechanisms for bleeding diatheses, but it is unknown whether placental, decidual immune cells or other abnormalities at the maternal-fetal interface contribute to FNAIT. Here we show that maternal immune responses to fetal platelet antigens cause miscarriage and IUGR that are associated with vascular and immune pathologies in murine FNAIT models. Uterine natural killer (uNK) cell recruitment and survival beyond mid-gestation lead to elevated NKp46 and CD107 expression, perforin release and trophoblast apoptosis. Depletion of NK cells restores normal spiral artery remodeling and placental function, prevents miscarriage, and rescues hemorrhage in neonates. Blockade of NK activation receptors (NKp46, FcɣRIIIa) also rescues pregnancy loss. These findings shed light on uNK antibody-dependent cell-mediated cytotoxicity of invasive trophoblasts as a pathological mechanism in FNAIT, and suggest that anti-NK cell therapies may prevent immune-mediated pregnancy loss and ameliorate FNAIT.Fetal/neonatal alloimmune thrombocytopenia (FNAIT) is a gestational disease caused by maternal immune responses against fetal platelets. Using a FNAIT mouse model and human trophoblast cell lines, here the authors show that uterine natural killer cell-mediated trophoblast apoptosis contributes to FNAIT pathogenesis.
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