ArticleImmunity2014
The oncoprotein and transcriptional regulator Bcl-3 governs plasticity and pathogenicity of autoimmune T cells.
Article in Immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
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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
25 citing papers in PubMed, 46 citations in OpenAlex.
- Unveiling the multifaceted roles of BCL3: biological functions and disease implications.Apoptosis : an international journal on programmed cell death · 2026Review
- Predictive modeling of molecular activity underlying physical cell-cell interactions.Cell reports methods · 2026Article
- Direct-in-NOD genetic ablation of Bcl3 leads to complete type 1 diabetes protection.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Regulation and Function of the Atypical IκBs-Bcl-3, IκBEuropean journal of immunology · 2025Review
- Roles of deubiquitinases in urologic cancers (Review).Oncology letters · 2024Review
- B-cell-derived IL-10 promotes allergic sensitization in asthma regulated by Bcl-3.Cellular & molecular immunology · 2023Article
- Bcl-3 regulates T cell function through energy metabolism.BMC immunology · 2023Article
- A systematic comparison of FOSL1, FOSL2 and BATF-mediated transcriptional regulation during early human Th17 differentiation.Nucleic acids research · 2022Article
- LPS/Bcl3/YAP1 signaling promotes Sox9Cell death & disease · 2022Article
- Bcl-3 regulates the function of Th17 cells through raptor mediated glycolysis metabolism.Frontiers in immunology · 2022Article
- Bcl-3: A Double-Edged Sword in Immune Cells and Inflammation.Frontiers in immunology · 2022Review
- Bcl-3 suppresses differentiation of RORγtImmunology and cell biology · 2021Article
- The neutrophil antimicrobial peptide cathelicidin promotes Th17 differentiation.Nature communications · 2021Article
- The NF-κB regulator Bcl-3 restricts terminal differentiation and promotes memory cell formation of CD8+ T cells during viral infection.PLoS pathogens · 2021Article
- The role of B-Cell Lymphoma-3 (BCL-3) in enabling the hallmarks of cancer: implications for the treatment of colorectal carcinogenesis.Carcinogenesis · 2020Review
- Expression of STAT3-regulated genes in circulating CD4+ T cells discriminates rheumatoid arthritis independently of clinical parameters in early arthritis.Rheumatology (Oxford, England) · 2019Article
- Antler extracts stimulate chondrocyte proliferation and possess potent anti-oxidative, anti-inflammatory, and immune-modulatory properties.In vitro cellular & developmental biology. Animal · 2018Article
- Nuclear Factor-kappaB in Autoimmunity: Man and Mouse.Frontiers in immunology · 2018Review
- Elevated levels of Bcl-3 inhibits Treg development and function resulting in spontaneous colitis.Nature communications · 2017Article
- The B-cell tumor promoter Bcl-3 suppresses inflammation-associated colon tumorigenesis in epithelial cells.Oncogene · 2016Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Bcl-3 is an atypical member of the IκB family that modulates transcription in the nucleus via association with p50 (NF-κB1) or p52 (NF-κB2) homodimers. Despite evidence attesting to the overall physiologic importance of Bcl-3, little is known about its cell-specific functions or mechanisms. Here we demonstrate a T-cell-intrinsic function of Bcl-3 in autoimmunity. Bcl-3-deficient T cells failed to induce disease in T cell transfer-induced colitis and experimental autoimmune encephalomyelitis. The protection against disease correlated with a decrease in Th1 cells that produced the cytokines IFN-γ and GM-CSF and an increase in Th17 cells. Although differentiation into Th1 cells was not impaired in the absence of Bcl-3, differentiated Th1 cells converted to less-pathogenic Th17-like cells, in part via mechanisms involving expression of the RORγt transcription factor. Thus, Bcl-3 constrained Th1 cell plasticity and promoted pathogenicity by blocking conversion to Th17-like cells, revealing a unique type of regulation that shapes adaptive immunity.
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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.