ArticleThe Journal of experimental medicine2014
Germinal center B cell maintenance and differentiation are controlled by distinct NF-κB transcription factor subunits.
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 139 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
139 citing papers in PubMed, 1 synthesis or guideline pooled it, 210 citations in OpenAlex.
- Genome-wide association study implicates immune dysfunction in the development of Hodgkin lymphoma.Blood · 2018Pooled it
- The Myeloma Risk Variant of TNFRSF13B Shows Reduced NF-κB Signalling Activity in HEK293 Cells.European journal of haematology · 2026Article
- Neutrophil-epithelial niches arrest B-cell maturation in dysfunctional tertiary lymphoid structures of gastric cancer neoadjuvant immunochemotherapy.Journal for immunotherapy of cancer · 2026Article
- Tensor network-based gene regulatory network inference for single-cell transcriptomic data.iScience · 2026Article
- Protocol for an in vivo CRISPR screen for germinal center B cells in mice using ecotropic retrovirus.STAR protocols · 2026Article
- Article
- The NF-κB transcription factor RelA directs mucosal-associated invariant T-cell development.Immunology and cell biology · 2026Article
- NF-κB-driven lymphangiogenesis affects kidney function via a VEGFR-3-mediated pathway.JCI insight · 2026Article
- Strong constitutive NF-κB signaling in B cells drives SLL/CLL-like lymphomagenesis and overcomes microenvironmental dependencies.Leukemia · 2026Article
- Mouse models of B cell lymphomas on the basis of genetic features.Frontiers in immunology · 2026Review
- Article
- c-Rel drives pancreatic cancer metastasis through fibronectin-integrin signaling-induced isolation stress resistance and EMT.Molecular cancer · 2025Article
- Genetic deregulation of REL in germinal center B cells induces generation of a pool of lymphoma precursor cells.Blood advances · 2025Article
- Pre-existing epigenetic state and differential NF-κB activation shape type 2 immune cell responses.Immunity · 2025Article
- Targeting inflammation in cancer therapy: from mechanistic insights to emerging therapeutic approaches.Journal of translational medicine · 2025Review
- Endothelial c-REL orchestrates atherosclerosis at regions of disturbed flow through crosstalk with TXNIP-p38 and non-canonical NF-κB pathways.Cardiovascular research · 2025Article
- TRAF3 loss protects glioblastoma cells from lipid peroxidation and immune elimination via dysregulated lipid metabolism.The Journal of clinical investigation · 2025Article
- Activation-induced cytidine deaminase in tertiary lymphoid structures: dual roles and implications in cancer prognosis.Frontiers in oncology · 2025Review
- Clearance of p21 highly expressing senescent cells accelerates cutaneous wound healing.Nature aging · 2025Article
- Focal adhesion kinase plays an essential role in Th17 cell differentiation by stimulating NF-κB signaling.Frontiers in immunology · 2025Article
79 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Germinal centers (GCs) are the sites where memory B cells and plasma cells producing high-affinity antibodies are generated during T cell-dependent immune responses. The molecular control of GC B cell maintenance and differentiation remains incompletely understood. Activation of the NF-κB signaling pathway has been implicated; however, the distinct roles of the individual NF-κB transcription factor subunits are unknown. We report that GC B cell-specific deletion of the NF-κB subunits c-REL or RELA, which are both activated by the canonical NF-κB pathway, abolished the generation of high-affinity B cells via different mechanisms acting at distinct stages during the GC reaction. c-REL deficiency led to the collapse of established GCs immediately after the formation of dark and light zones at day 7 of the GC reaction and was associated with the failure to activate a metabolic program that promotes cell growth. Conversely, RELA was dispensable for GC maintenance but essential for the development of GC-derived plasma cells due to impaired up-regulation of BLIMP1. These results indicate that activation of the canonical NF-κB pathway in GC B cells controls GC maintenance and differentiation through distinct transcription factor subunits. Our findings have implications for the role of NF-κB in GC lymphomagenesis.
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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.