ArticleThe Journal of experimental medicine2021
Exit from germinal center to become quiescent memory B cells depends on metabolic reprograming and provision of a survival signal.
Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 75 citations in OpenAlex.
- Autophagy determines the fate of immune cells by regulating metabolic remodeling and PANoptosis (Review).International journal of molecular medicine · 2026Review
- BRWD1 directs B cell epigenetic states required for germinal center initiation, maintenance and function.Nature communications · 2026Article
- Plasma Cell Selection and Migration in the Establishment of Long-Lived Antibody Responses.Immunological reviews · 2026Review
- Interferon-Mediated Regulation of Memory B Cell Identity and Function.Immunological reviews · 2026Review
- Cytoskeletal Protein 4.1R Inhibits BCR-Mediated B-Cell Activation by Restraining AKT1 Phosphorylation.Cells · 2026Article
- Affinity- and epitope-dependent pathogenicity of GM-CSF autoantibodies in patients with autoimmune pulmonary alveolar proteinosis.Nature communications · 2026Article
- Antibody-mediated diversification of primary and secondary humoral immune responses.The Journal of experimental medicine · 2026Article
- The B cell receptor-mTOR signaling axis restricts the accumulation of lung tissue-resident memory B cells after influenza infection.Science immunology · 2026Article
- The multilayered identity of B cell memory.Cellular & molecular immunology · 2026Review
- Antibody Mediated Diversification of Primary and Secondary Immune Responses.bioRxiv : the preprint server for biology · 2025Article
- Identification and experimental validation of biomarkers associated with the endocannabinoid system in major depressive disorder.Hereditas · 2025Article
- PCV2 Infection Represses the Differentiation of Light Zone Germinal Center B Cells by Inhibiting Their Interaction with Helper Cells.Microorganisms · 2025Article
- Clonal expansion and diversification of germinal center and memory B cell responses to booster immunization in primates.Cell reports · 2025Article
- BLIMP1 controls GC B cell expansion and exit through regulating cell cycle progression and key transcription factors BCL6 and IRF4.Cell reports · 2025Article
- Clonal Expansion and Diversification of Germinal Center and Memory B Cell Responses to Booster Immunization in Primates.bioRxiv : the preprint server for biology · 2025Article
- From powerhouse to modulator: regulating immune system responses through intracellular mitochondrial transfer.Cell communication and signaling : CCS · 2025Review
- KLF2 expression in IgG plasma cells at their induction site regulates the migration program.The Journal of experimental medicine · 2025Article
- Polarization of the memory B-cell response.Journal of leukocyte biology · 2025Review
- Sex-specific molecular signature of mouse podocytes in homeostasis and in response to pharmacological challenge with rapamycin.Biology of sex differences · 2024Article
- Maf expression in B cells restricts reactive plasmablast and germinal center B cell expansion.Nature communications · 2024Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A still unanswered question is what drives the small fraction of activated germinal center (GC) B cells to become long-lived quiescent memory B cells. We found here that a small population of GC-derived CD38intBcl6hi/intEfnb1+ cells with lower mTORC1 activity favored the memory B cell fate. Constitutively high mTORC1 activity led to defects in formation of the CD38intBcl6hi/intEfnb1+ cells; conversely, decreasing mTORC1 activity resulted in relative enrichment of this memory-prone population over the recycling-prone one. Furthermore, the CD38intBcl6hi/intEfnb1+ cells had higher levels of Bcl2 and surface BCR that, in turn, contributed to their survival and development. We also found that downregulation of Bcl6 resulted in increased expression of both Bcl2 and BCR. Given the positive correlation between the strength of T cell help and mTORC1 activity, our data suggest a model in which weak help from T cells together with provision of an increased survival signal are key for GC B cells to adopt a memory B cell fate.
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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.