ArticleThe Journal of experimental medicine2014
The transcription factors IRF8 and PU.1 negatively regulate plasma cell differentiation.
Article in The Journal of experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 2 of them syntheses that pooled it.
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
96 citing papers in PubMed, 2 syntheses or guidelines pooled it, 146 citations in OpenAlex.
- GWAS for systemic sclerosis identifies six novel susceptibility loci including one in the Fcγ receptor region.Nature communications · 2024Pooled it
- The diversity of the plasmablast signature across species and experimental conditions: A meta-analysis.Immunology · 2021Pooled it
- Review
- Integrated Genomic and Epigenomic Analysis Reveals Epigenetic Plasticity in Disease Progression and Multidrug Resistance in Multiple Myeloma.Cancer research · 2026Article
- Artery tertiary lymphoid organs encode a pathogenic high-affinity autoantibody-autoantigen pair in atherosclerosis.Nature cardiovascular research · 2026Article
- The transcription factor IRF8 drives tumor-specific exhaustion in CD8+ T cells.The Journal of experimental medicine · 2026Article
- Competing gene regulatory networks drive naive and memory B cell differentiation.Molecular systems biology · 2026Article
- Pharmacological targeting of IRF4 as a therapeutic strategy for multiple myeloma.Nature chemical biology · 2026Article
- IFNγ-induced IRF1 synergizes with TLR7 signals to tune the IRF4-IRF8 axis and drive pathogenic effector B cell fate.bioRxiv : the preprint server for biology · 2026Article
- The pathogenic role of double-negative B cells in autoimmune diseases.Frontiers in immunology · 2026Review
- Article
- Epigenetic Plasticity Drives Carcinogenesis and Multi-Therapy Resistance in Multiple Myeloma.Research square · 2025Article
- A Csde1-Strap complex regulates plasma cell differentiation by coupling mRNA translation and decay.Nature communications · 2025Article
- Predicting and comparing transcription start sites in single cell populations.PLoS computational biology · 2025Article
- CD11c-Cre driven deletion ofFrontiers in immunology · 2025Article
- Langerhans cells drive Tfh and B cell responses independent of canonical cytokine signals.Frontiers in immunology · 2025Article
- ETS Transcription Factors in Immune Cells and Immune-Related Diseases.International journal of molecular sciences · 2024Review
- PI3Kγ in B cells promotes antibody responses and generation of antibody-secreting cells.Nature immunology · 2024Article
- IRF8-mutant B cell lymphoma evades immunity through a CD74-dependent deregulation of antigen processing and presentation in MHCII complexes.Science advances · 2024Article
- Article
36 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
Activated B cells undergo immunoglobulin class-switch recombination (CSR) and differentiate into antibody-secreting plasma cells. The distinct transcriptomes of B cells and plasma cells are maintained by the antagonistic influences of two groups of transcription factors: those that maintain the B cell program, including BCL6 and PAX5, and plasma cell-promoting factors, such as IRF4 and BLIMP-1. We show that the complex of IRF8 and PU.1 controls the propensity of B cells to undergo CSR and plasma cell differentiation by concurrently promoting the expression of BCL6 and PAX5 and repressing AID and BLIMP-1. As the PU.1-IRF8 complex functions in a reciprocal manner to IRF4, we propose that concentration-dependent competition between these factors controls B cell terminal differentiation.
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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.