ArticleJournal of immunology (Baltimore, Md. : 1950)2014
BCL6 controls Th9 cell development by repressing Il9 transcription.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 53 citations in OpenAlex.
- Loss of YTHDF2 enhances Th9 programming and CAR-Th9 cell antitumor efficacy.Nature immunology · 2025Article
- Targeting Th9 cells in autoimmune diseases: a narrative review.Frontiers in immunology · 2025Review
- B Cell Lymphoma 6 (BCL6): A Conserved Regulator of Immunity and Beyond.International journal of molecular sciences · 2024Review
- Locus of (IL-9) control: IL9 epigenetic regulation in cellular function and human disease.Experimental & molecular medicine · 2024Review
- TXA2 attenuates allergic lung inflammation through regulation of Th2, Th9, and Treg differentiation.The Journal of clinical investigation · 2024Article
- T-helper cells flexibility: the possibility of reprogramming T cells fate.Frontiers in immunology · 2023Review
- IL-1β promotes IL-9-producing Th cell differentiation in IL-2-limiting conditions through the inhibition of BCL6.Frontiers in immunology · 2022Article
- B cell lymphoma 6A regulates immune development and function in zebrafish.Frontiers in cellular and infection microbiology · 2022Article
- STAT5 Represses a STAT3-Independent Th17-like Program during Th9 Cell Differentiation.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Critical Roles of Balanced T Helper 9 Cells and Regulatory T Cells in Allergic Airway Inflammation and Tumor Immunity.Journal of immunology research · 2021Review
- ZBTB Transcription Factors: Key Regulators of the Development, Differentiation and Effector Function of T Cells.Frontiers in immunology · 2021Review
- Proteome analysis revealed the essential functions of protein phosphatase PP2A in the induction of Th9 cells.Scientific reports · 2020Article
- BCL-6 suppresses miR-142-3p/5p expression in SLE CD4Cellular & molecular immunology · 2020Article
- Opposite functions of STAT3 and Smad3 in regulating Tiam1 expression in Th17 cells.Small GTPases · 2020Article
- BATF-Interacting Proteins Dictate Specificity in Th Subset Activity.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Transcription factor networks in aged naïve CD4 T cells bias lineage differentiation.Aging cell · 2019Article
- A conserved enhancer regulates Il9 expression in multiple lineages.Nature communications · 2018Article
- Metabolic Checkpoints in Differentiation of Helper T Cells in Tissue Inflammation.Frontiers in immunology · 2018Review
- Foxo1 and Foxp1 play opposing roles in regulating the differentiation and antitumor activity of TScience signaling · 2017Article
- Paracrine IL-2 Is Required for Optimal Type 2 Effector Cytokine Production.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The transcriptional repressor B cell lymphoma 6 (BCL6) is required for the development of Th follicular cells, and it has been shown to suppress Th2 cell differentiation. We demonstrate that BCL6 is a key regulator of Th9 cell development. BCL6 expression is transiently downregulated in polarized Th9 cells, and forced expression of BCL6 in Th9 cells impairs Th9 cell differentiation. In contrast, BCL6 knockdown upregulated IL-9 production in Th9 cells. The function of BCL6 in Th9 cells is under the control of IL-2/JAK3/STAT5 signaling pathway. Using chromatin immunoprecipitation, we show that, in Th9 cells, BCL6 and STAT5 bind to adjacent motifs in the Il9 promoter. Furthermore, we found that STAT5 binding was associated with the abundance of a permissive histone mark at the Il9 promoter, whereas under conditions in which BCL6 binding was predominant, a repressive histone mark was prevalent. The effects of STAT5 and BCL6 on IL-9 transcription were further demonstrated using an IL-9 luciferase reporter assay in which BCL6 repressed STAT5-mediated Il9 transactivation. In experimental autoimmune encephalomyelitis, forced expression of BCL6 in myelin oligodendrocyte glycoprotein35-55-specific Th9 cells resulted in decreased IL-9 production and induction of IFN-γ, causing an exacerbation of the clinical disease. Our findings demonstrate a novel role of BCL6 in the regulation of Th9 cell development and their encephalitogenicity.
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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.