ArticleImmunity2007
A role for the IkappaB family member Bcl-3 in the control of central immunologic tolerance.
Article in Immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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.
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Who cites it
47 citing papers in PubMed, 74 citations in OpenAlex.
- Differential NF-kappaB pathways induction by Lactobacillus plantarum in the duodenum of healthy humans correlating with immune tolerance.Proceedings of the National Academy of Sciences of the United States of America · 2009Trial
- Single-cell transcriptomic profiling reveals diversity in human iNKT cells across hematologic tissues.Cell reports · 2025Article
- Regulation and Function of the Atypical IκBs-Bcl-3, IκBEuropean journal of immunology · 2025Review
- Skewed epithelial cell differentiation and premature aging of the thymus in the absence of vitamin D signaling.Science advances · 2024Article
- The role of regulatory B cells in immune regulation and childhood allergic asthma.Molecular and cellular pediatrics · 2024Review
- B-cell-derived IL-10 promotes allergic sensitization in asthma regulated by Bcl-3.Cellular & molecular immunology · 2023Article
- Regulation of IkappaB Protein Expression by Early Gestation in the Thymus of Ewes.Veterinary sciences · 2023Article
- NF kappa B regulator Bcl3 controls development and function of classical dendritic cells required for resistance to Toxoplasma gondii.PLoS pathogens · 2022Article
- Bcl-3 promotes TNF-induced hepatocyte apoptosis by regulating the deubiquitination of RIP1.Cell death and differentiation · 2022Article
- LPS/Bcl3/YAP1 signaling promotes Sox9Cell death & disease · 2022Article
- Atypical IκB Bcl3 enhances the generation of the NF-κB p52 homodimer.Frontiers in cell and developmental biology · 2022Article
- Bcl-3: A Double-Edged Sword in Immune Cells and Inflammation.Frontiers in immunology · 2022Review
- Epigenetic modifications in thymic epithelial cells: an evolutionary perspective for thymus atrophy.Clinical epigenetics · 2021Review
- Bcl-3 suppresses differentiation of RORγtImmunology and cell biology · 2021Article
- Origin of the Functional Distinctiveness of NF-κB/p52.Frontiers in cell and developmental biology · 2021Review
- NF-κB: At the Borders of Autoimmunity and Inflammation.Frontiers in immunology · 2021Review
- The NF-κB regulator Bcl-3 restricts terminal differentiation and promotes memory cell formation of CD8+ T cells during viral infection.PLoS pathogens · 2021Article
- Thymic Epithelial Cells Contribute to Thymopoiesis and T Cell Development.Frontiers in immunology · 2019Review
- Alternative NF-κB signaling promotes colorectal tumorigenesis through transcriptionally upregulating Bcl-3.Oncogene · 2018Article
- Bcl3 Phosphorylation by Akt, Erk2, and IKK Is Required for Its Transcriptional Activity.Molecular cell · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Bcl-3 is a member of the family of IkappaB inhibitors. Unlike the classical, cytoplasmic IkappaBs, Bcl-3 does not inhibit RelA- or c-Rel-containing NF-kappaB transcription factor dimers. Instead, Bcl-3 can enter the nucleus and modulate NF-kappaB activity, although the underlying mechanism and physiologic function remain largely unknown. Here we identified Bcl-3 as a regulator of immunologic tolerance to self. In parallel with NF-kappaB2, Bcl-3 functions within stroma to generate medullary thymic epithelial cells, which are essential for negative selection of autoreactive T cells. Loss of both NF-kappaB2 and Bcl-3, but not either one alone, led to a profound breakdown in central tolerance resulting in rapid and fatal multiorgan inflammation. These data reveal extensive utilization of the NF-kappaB system to promote central tolerance in the thymus, in apparent contrast with the well-known roles of NF-kappaB to promote inflammation and autoimmunity in the periphery.
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What OpenQuestion holds
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.