ArticleThe Journal of allergy and clinical immunology2023
RelB-deficient autoinflammatory pathology presents as interferonopathy, but in mice is interferon-independent.
Article in The Journal of allergy and clinical immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- NF-κB inducing kinase (NIK) deletion accelerates KRAS-driven pancreatic cancer in association with tumor microenvironment remodeling.Cell death & disease · 2026Article
- IRAK2 deficiency causes immune dysregulation through defective Myddosome assembly and enhanced interferon responses.Nature communications · 2026Article
- Distinct roles for NF-κB in hematopoietic stem cells and the bone marrow milieu in promoting hematopoietic aging.Cell reports · 2025Article
- Dendritic cell maturation in cancer.Nature reviews. Cancer · 2025Review
- NF-κB RelB suppresses the inflammatory gene expression programs of dendritic cells by competing with RelA for binding to target gene promoters.Cell discovery · 2025Article
- Inborn Errors of Immunity Presenting with Early-Onset Severe Atopy.Medicina (Kaunas, Lithuania) · 2025Review
- NF-κB: master regulator of cellular responses in health and disease.Immunity & inflammation · 2025Review
- Defective kinase activity of IKKα leads to combined immunodeficiency and disruption of immune tolerance in humans.Nature communications · 2024Article
- Non-canonical NF-κB signaling limits the tolerogenic β-catenin-Raldh2 axis in gut dendritic cells to exacerbate intestinal pathologies.The EMBO journal · 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
- Deciphering NF-kappaB pathways in smoking-related lung carcinogenesis.EXCLI journal · 2024Review
- The noncanonical NFκB pathway: Regulatory mechanisms in health and disease.WIREs mechanisms of diseaseReview
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundAutoimmune diseases are leading causes of ill health and morbidity and have diverse etiology. Two signaling pathways are key drivers of autoimmune pathology, interferon and nuclear factor-κB (NF-κB)/RelA, defining the 2 broad labels of interferonopathies and relopathies. Prior work has established that genetic loss of function of the NF-κB subunit RelB leads to autoimmune and inflammatory pathology in mice and humans.
objectiveWe sought to characterize RelB-deficient autoimmunity by unbiased profiling of the responses of immune sentinel cells to stimulus and to determine the functional role of dysregulated gene programs in the RelB-deficient pathology.
methodsTranscriptomic profiling was performed on fibroblasts and dendritic cells derived from patients with RelB deficiency and knockout mice, and transcriptomic responses and pathology were assessed in mice deficient in both RelB and the type I interferon receptor.
resultsWe found that loss of RelB in patient-derived fibroblasts and mouse myeloid cells results in elevated induction of hundreds of interferon-stimulated genes. Removing hyperexpression of the interferon-stimulated gene program did not ameliorate the autoimmune pathology of RelB knockout mice. Instead, we found that RelB suppresses a different set of inflammatory response genes in a manner that is independent of interferon signaling but associated with NF-κB binding motifs.
conclusionAlthough transcriptomic profiling would describe RelB-deficient autoimmune disease as an interferonopathy, the genetic evidence indicates that the pathology in mice is interferon-independent.
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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.