ArticleThe Journal of experimental medicine2016
NFκB1 is essential to prevent the development of multiorgan autoimmunity by limiting IL-6 production in follicular B cells.
Article in The Journal of experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Mice lacking NF-ĸB1 undergo premature ovarian aging.Reproductive biology and endocrinology : RB&E · 2026Article
- B Cell Subsets and Atherosclerosis: Updates and Emerging Concepts.Immunological reviews · 2026Review
- The NF-κB1/p50 Subunit Influences the Notch/IL-6-Driven Expansion of Myeloid-Derived Suppressor Cells in Murine T-Cell Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2024Article
- Age-associated B cells predict impaired humoral immunity after COVID-19 vaccination in patients receiving immune checkpoint blockade.Nature communications · 2023Article
- NF-κB Mutations in Germinal Center B-Cell Lymphomas: Relation to NF-κB Function in Normal B Cells.Biomedicines · 2022Review
- NF-κB and Pancreatic Cancer; Chapter and Verse.Cancers · 2021Review
- Virus Infection Induces Keap1 Binding to Cytokine Genes, Which Recruits NF-κB p50 and G9a-GLP and Represses Cytokine Transcription.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- The ocular surface immune system through the eyes of aging.The ocular surface · 2021Review
- Moderate Exercise Inhibits Age-Related Inflammation, Liver Steatosis, Senescence, and Tumorigenesis.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Nuclear Factor κB (NF-κB)-Mediated Inflammation in Multiple Sclerosis.Frontiers in immunology · 2020Review
- Non-Antibody-Secreting Functions of B Cells and Their Contribution to Autoimmune Disease.Annual review of cell and developmental biology · 2019Review
- Activating mutations in PIK3CD disrupt the differentiation and function of human and murine CD4The Journal of allergy and clinical immunology · 2019Article
- Molecular regulation of peripheral B cells and their progeny in immunity.Genes & development · 2019Review
- IL-6: a cytokine at the crossroads of autoimmunity.Current opinion in immunology · 2018Review
- Review
- Nuclear Factor-kappaB in Autoimmunity: Man and Mouse.Frontiers in immunology · 2018Review
- B cell-derived IL-6 initiates spontaneous germinal center formation during systemic autoimmunity.The Journal of experimental medicine · 2017Article
- The Pathophysiology of Dry Eye Disease: What We Know and Future Directions for Research.Ophthalmology · 2017Review
- NF-κB p50 (Blood · 2017Article
- Altered B cell signalling in autoimmunity.Nature reviews. Immunology · 2017Review
Corrections and comments
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Authors and funding
20 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We examined the role of NFκB1 in the homeostasis and function of peripheral follicular (Fo) B cells. Aging mice lacking NFκB1 (Nfκb1(-/-)) develop lymphoproliferative and multiorgan autoimmune disease attributed in large part to the deregulated activity of Nfκb1(-/-)Fo B cells that produce excessive levels of the proinflammatory cytokine interleukin 6 (IL-6). Despite enhanced germinal center (GC) B cell differentiation, the formation of GC structures was severely disrupted in the Nfκb1(-/-)mice. Bone marrow chimeric mice revealed that the Fo B cell-intrinsic loss of NFκB1 led to the spontaneous generation of GC B cells. This was primarily the result of an increase in IL-6 levels, which promotes the differentiation of Fo helper CD4(+)T cells and acts in an autocrine manner to reduce antigen receptor and toll-like receptor activation thresholds in a population of proliferating IgM(+)Nfκb1(-/-)Fo B cells. We demonstrate that p50-NFκB1 represses Il-6 transcription in Fo B cells, with the loss of NFκB1 also resulting in the uncontrolled RELA-driven transcription of Il-6.Collectively, our findings identify a previously unrecognized role for NFκB1 in preventing multiorgan autoimmunity through its negative regulation of Il-6 gene expression in Fo B cells.
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