ArticleDevelopment (Cambridge, England)2022
Erythro-myeloid progenitor origin of Hofbauer cells in the early mouse placenta.
Article in Development (Cambridge, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Gestational Dynamics of Hofbauer Cells in the Human Placenta: Distribution, Morphology, and Immunophenotype.Journal of developmental biology · 2026Article
- Article
- The maternal-fetal interface at single-cell resolution: uncovering the cellular anatomy of the placenta and decidua.American journal of obstetrics and gynecology · 2025Review
- AssessingFrontiers in immunology · 2025Review
- Fetal MAVS and type I IFN signaling pathways control ZIKV infection in the placenta and maternal decidua.The Journal of experimental medicine · 2024Article
- Hofbauer cells and fetal brain microglia share transcriptional profiles and responses to maternal diet-induced obesity.Cell reports · 2024Article
- The immune landscape of fetal chorionic villous tissue in term placenta.Frontiers in immunology · 2024Article
- Tissue-specific macrophages: how they develop and choreograph tissue biology.Nature reviews. Immunology · 2023Review
- Bioinformatics analysis of potential pathogenesis and risk genes of immunoinflammation-promoted renal injury in severe COVID-19.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hofbauer cells (HBCs) are tissue macrophages of the placenta thought to be important for fetoplacental vascular development and innate immune protection. The developmental origins of HBCs remain unresolved and could implicate functional diversity of HBCs in placenta development and disease. In this study, we used flow cytometry and paternally inherited reporters to phenotype placenta macrophages and to identify fetal-derived HBCs and placenta-associated maternal macrophages in the mouse. In vivo pulse-labeling traced the ontogeny of HBCs from yolk sac-derived erythro-myeloid progenitors, with a minor contribution from fetal hematopoietic stem cells later on. Single-cell RNA-sequencing revealed transcriptional similarities between placenta macrophages and erythro-myeloid progenitor-derived fetal liver macrophages and microglia. As with other fetal tissue macrophages, HBCs were dependent on the transcription factor Pu.1, the loss-of-function of which in embryos disrupted fetoplacental labyrinth morphology, supporting a role for HBC in labyrinth angiogenesis and/or remodeling. HBC were also sensitive to Pu.1 (Spi1) haploinsufficiency, which caused an initial deficiency in the numbers of macrophages in the early mouse placenta. These results provide groundwork for future investigation into the relationship between HBC ontogeny and function in placenta pathophysiology.
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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.