ArticleThe Journal of experimental medicine2000
Precursor B cell receptor-dependent B cell proliferation and differentiation does not require the bone marrow or fetal liver environment.
Article in The Journal of experimental medicine, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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
55 citing papers in PubMed, 173 citations in OpenAlex.
- IKAROS isoforms differentially control gene expression and differentiation of a B-cell acute lymphoblastic leukemia cell line.Nagoya journal of medical science · 2026Article
- Overview of the Different Classes of Small RNAs During B-Cell Development.Methods in molecular biology (Clifton, N.J.) · 2025Review
- Maternal Helminth Infection Causes Dysfunctional B Cell Development in Male Offspring.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Concepts in B cell acute lymphoblastic leukemia pathogenesis.Journal of leukocyte biology · 2024Review
- Intragraft B cell differentiation during the development of tolerance to kidney allografts is associated with a regulatory B cell signature revealed by single cell transcriptomics.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2023Article
- ATP11C promotes the differentiation of pre-B cells into immature B cells but does not affect their IL-7-dependent proliferation.Immunologic research · 2023Article
- Article
- Evolution of surrogate light chain in tetrapods and the relationship between lengths of CDR H3 and VpreB tails.Frontiers in immunology · 2022Article
- Comparative Aspects of Immunoglobulin Gene Rearrangement Arrays in Different Species.Frontiers in immunology · 2022Review
- It Takes Three Receptors to Raise a B Cell.Trends in immunology · 2020Review
- Article
- RAG-Mediated DNA Breaks Attenuate PU.1 Activity in Early B Cells through Activation of a SPIC-BCLAF1 Complex.Cell reports · 2019Article
- Cell circuits and niches controlling B cell development.Immunological reviews · 2019Review
- From zero to sixty and back to zero again: the metabolic life of B cells.Current opinion in immunology · 2019Review
- The Majority of CD45Immunity · 2018Article
- Immunosuppression in Experimental Chagas Disease Is Mediated by an Alteration of Bone Marrow Stromal Cell Function During the Acute Phase of Infection.Frontiers in immunology · 2018Article
- The Role of the Pre-B Cell Receptor in B Cell Development, Repertoire Selection, and Tolerance.Frontiers in immunology · 2018Review
- Ibrutinib inhibits pre-BCRBlood · 2017Article
- RAG-mediated DNA double-strand breaks activate a cell type-specific checkpoint to inhibit pre-B cell receptor signals.The Journal of experimental medicine · 2016Article
- Emerging Functions of Natural IgM and Its Fc Receptor FCMR in Immune Homeostasis.Frontiers in immunology · 2016Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The capacity of precursor B (pre-B) I cells from fetal liver and bone marrow to proliferate and differentiate into surface immunoglobulin-positive immature B cells in vitro was analyzed. Both fetal liver- and bone marrow-derived progenitors do so in a pre-B cell receptor (pre-BCR)-dependent manner in tissue culture medium alone, without addition of other cells or cytokines. Approximately 20% of the initial pre-B I cells enter more than one division. Analyses at the single-cell level show that approximately 15% divide two to five times. Coculture of pre-B I cells with stromal cells did not enhance proliferation or differentiation, whereas the presence of interleukin 7, especially in combination with stromal cells, resulted mainly in the expansion of pre-B I cells and prevented their further differentiation. Thus, the environment of fetal liver or bone marrow is not required for the pre-BCR to exert its function, which is to select and expand cells that have undergone an inframe V(H)-D(H)J(H) rearrangement that produces a pre-BCR-compatible muH chain. It appears unlikely that a ligand for the pre-BCR drives this pre-B cell proliferation.
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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.