ArticleFrontiers in immunology2022
Mast Cell Repopulating Ability Is Lost During the Transition From Pre-HSC to FL HSC.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Hematopoietic stem cell-independent and -dependent hematopoiesis: new insights and lineage-tracing methods.Experimental hematology · 2026Review
- Mast Cells Are Not Essential for Pubertal Mammary Gland Branching.European journal of immunology · 2025Article
- Regulation of HSC development and function by Lin28b.Frontiers in cell and developmental biology · 2025Review
- Mast cell ontogeny: From fetal development to life-long health and disease.Immunological reviews · 2023Review
- Multiple waves of fetal-derived immune cells constitute adult immune system.Immunological reviews · 2023Review
- The ins and outs of innate and adaptive type 2 immunity.Immunity · 2023Review
- HSC-independent definitive hematopoiesis persists into adult life.Cell reports · 2023Article
- Hematopoietic Stem Cells and the Immune System in Development and Aging.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Recent advances in developmental immunology have revealed a hematopoietic stem cell (HSC)-independent origin for various innate immune lineages, including mast cells (MCs). It is now established that adult bone marrow (BM) long-term HSCs do not regenerate MCs but, instead, the physiological production of MCs starts before the emergence of HSCs in the aorta-gonad-mesonephros (AGM) region and is mostly completed before birth. However, while the AGM region represents a major site of MC generation during ontogeny, whether the first emerging HSCs in the AGM or fetal liver (FL) possess the potential to regenerate MCs is unknown. Here, we combined three fate-mapping mouse models with detailed HSC transplantation assays to determine the potential of AGM and FL HSCs to produce MCs. We show that HSCs from E11.5 AGM and E12.5 FL efficiently repopulated MCs in recipients. In stark contrast, HSCs from ≥E14.5 FL failed to reconstitute MCs. An Endothelial (EC) fate-mapping study confirmed the EC origin of the majority of MCs. Additionally, our HSC-labeling showed that HSCs do not produce MCs in a physiological setting. Hence, although most MCs are generated and maintained
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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 Socratic graph.