ArticleImmunity2019
A Regulatory Circuit Controlling the Dynamics of NFκB cRel Transitions B Cells from Proliferation to Plasma Cell Differentiation.
Article in Immunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 84 citations in OpenAlex.
- Digital spatial profiling uncovers transcriptomic features of distinct plasma cell-like phenotypes in diffuse large B-cell lymphoma.Blood advances · 2026Article
- NF-κB-c-Rel in psoriasis: genetic susceptibility, immunopathogenic circuits, and emerging therapeutic opportunities.Frontiers in immunology · 2026Review
- Quantitative systems pharmacology model of B cell immune response in mouse.Frontiers in immunology · 2026Article
- Article
- Extrafollicular B Cell Responses-Is One Tent Big Enough?Immunological reviews · 2025Review
- Enforced MYC expression directs a distinct transcriptional state during plasma cell differentiation.Life science alliance · 2025Article
- Computational modelling of aggressive B-cell lymphoma.Biochemical Society transactions · 2025Review
- Synergy and antagonism in the integration of BCR and CD40 signals that control B-cell population expansion.Molecular systems biology · 2025Article
- Marginal zone and follicular B cells respond differently to TLR4 and TLR9 stimulation.bioRxiv : the preprint server for biology · 2025Article
- Linking signaling dynamics and cell fate decisions through single-cell imaging: evidence and challenges.Frontiers in cell and developmental biology · 2025Review
- Maf expression in B cells restricts reactive plasmablast and germinal center B cell expansion.Nature communications · 2024Article
- Tracking of lineage massLab on a chip · 2024Article
- Direct observation correlates NFκB cRel in B cells with activating and terminating their proliferative program.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Patient-specific computational models predict prognosis in B cell lymphoma by quantifying pro-proliferative and anti-apoptotic signatures from genetic sequencing data.Blood cancer journal · 2024Article
- A landscape of gene expression regulation for synovium in arthritis.Nature communications · 2024Article
- A multiscale spatial modeling framework for the germinal center response.Frontiers in immunology · 2024Article
- A computational model of the DNA damage-induced IKK/ NF-κB pathway reveals a critical dependence on irradiation dose and PARP-1.iScience · 2023Article
- Cytokine receptor IL27RA is an NF-κB-responsive gene involved in CD38 upregulation in multiple myeloma.Blood advances · 2023Article
- Toll-like receptor mediated inflammation directs B cells towards protective antiviral extrafollicular responses.Nature communications · 2023Article
- Computational modeling of DLBCL predicts response to BH3-mimetics.NPJ systems biology and applications · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Humoral immunity depends on efficient activation of B cells and their subsequent differentiation into antibody-secreting cells (ASCs). The transcription factor NFκB cRel is critical for B cell proliferation, but incorporating its known regulatory interactions into a mathematical model of the ASC differentiation circuit prevented ASC generation in simulations. Indeed, experimental ectopic cRel expression blocked ASC differentiation by inhibiting the transcription factor Blimp1, and in wild-type (WT) cells cRel was dynamically repressed during ASC differentiation by Blimp1 binding the Rel locus. Including this bi-stable circuit of mutual cRel-Blimp1 antagonism into a multi-scale model revealed that dynamic repression of cRel controls the switch from B cell proliferation to ASC generation phases and hence the respective cell population dynamics. Our studies provide a mechanistic explanation of how dysregulation of this bi-stable circuit might result in pathologic B cell population phenotypes and thus offer new avenues for diagnostic stratification and treatment.
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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.