ArticleNature immunology2024
Arid1a-dependent canonical BAF complex suppresses inflammatory programs to drive efficient germinal center B cell responses.
Article in Nature immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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
11 citing papers in PubMed.
- BPTF is essential for vaccine-induced germinal center B cell responses.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Role of PBAF and Mediator kinase module in the RELA-dependent activation ofFrontiers in immunology · 2026Article
- Capsaicin attenuates high-fat diet-induced impairment of B-cell immunity.SAGE open medicine · 2026Article
- Common cold embecovirus imprinting primes broadly neutralizing antibody responses to SARS-CoV-2 S2.The Journal of experimental medicine · 2025Article
- Review
- ARID1A and ARID1B preserve B cell identity, prevent myeloid transformation and reveal therapeutic vulnerabilities.bioRxiv : the preprint server for biology · 2025Article
- Targeting ARID1A: the key to dominating the differentiation fate of germinal center B cells.Science China. Life sciences · 2025Article
- Arid2 promotes Follicular B-cell differentiation and antibody responsesbioRxiv : the preprint server for biology · 2025Article
- CFP1 promotes germinal center affinity maturation and restrains memory B cell differentiation through H3K4me3 modulation.Nature communications · 2025Article
- Advances in molecular pathology and therapy of non-small cell lung cancer.Signal transduction and targeted therapy · 2025Review
- Chromatin remodeling in lymphocytic function and fate: the multifaceted roles of SWI/SNF complex.Frontiers in immunology · 2025Review
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12 authors.
Funding
Abstract
The mammalian Brg1/Brm-associated factor (BAF) complexes are major regulators of nucleosomal remodeling that are commonly mutated in several cancers, including germinal center (GC)-derived B cell lymphomas. However, the specific roles of different BAF complexes in GC B cell biology are not well understood. Here we show that the AT-rich interaction domain 1a (Arid1a) containing canonical BAF (cBAF) complex is required for maintenance of GCs and high-affinity antibody responses. While Arid1a-deficient B cells undergo initial activation, they fail to sustain the GC program. Arid1a establishes permissive chromatin landscapes for B cell activation and is concomitantly required to suppress inflammatory gene programs. The inflammatory signatures instigated by Arid1a deficiency promoted the recruitment of neutrophils and inflammatory monocytes. Dampening of inflammatory cues through interleukin-1β blockade or glucocorticoid receptor agonist partially rescued Arid1a-deficient GCs, highlighting a critical role for inflammation in impeding GCs. Our work reveals essential functions of Arid1a-dependent cBAF in promoting efficient GC responses.
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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.