ArticleNature communications2024
Peripheral apoptosis and limited clonal deletion during physiologic murine B lymphocyte development.
Article in Nature communications, 2024. 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed.
- Viral subversion of B-cell tolerance: mechanisms linking infection to autoimmunity.EMBO reports · 2026Review
- Rosa26-INDIA Identifies Early Apoptotic B Cells Before Macrophage-Mediated Efferocytosis.Immune network · 2026Article
- Distributed clonal deletion prevents autoimmune disease progression.Cell reports · 2026Article
- Distributed Clonal Deletion Prevents Autoimmune Disease Progression.bioRxiv : the preprint server for biology · 2026Article
- Proteasome alteration between epithelial and hematopoietic cells facilitates positive selection of CD8 T cells.Nature communications · 2026Article
- Regulatory B Cells at the Crossroads of Epigenetic Control and Immune Homeostasis.Clinical reviews in allergy & immunology · 2026Review
- Unlocking the Secrets of Regulated Cell Death in Large B-Cell Lymphoma Beyond Apoptosis: Signaling Pathways and Therapeutic Options.International journal of molecular sciences · 2026Review
- Distributed apoptotic checkpoints in B cell selection, tolerance, and autoimmunity.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Self-reactive and polyreactive B cells generated during B cell development are silenced by either apoptosis, clonal deletion, receptor editing or anergy to avoid autoimmunity. The specific contribution of apoptosis to normal B cell development and self-tolerance is incompletely understood. Here, we quantify self-reactivity, polyreactivity and apoptosis during physiologic B lymphocyte development. Self-reactivity and polyreactivity are most abundant in early immature B cells and diminish significantly during maturation within the bone marrow. Minimal apoptosis still occurs at this site, however B cell receptors cloned from apoptotic B cells show comparable self-reactivity to that of viable cells. Apoptosis increases dramatically only following immature B cells leaving the bone marrow sinusoids, but above 90% of cloned apoptotic transitional B cells are not self-reactive/polyreactive. Our data suggests that an apoptosis-independent mechanism, such as receptor editing, removes most self-reactive B cells in the bone marrow. Mechanistically, lack of survival signaling rather than clonal deletion appears to be the underpinning cause of apoptosis in most transitional B cells in the periphery.
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Registered trials
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