ArticleThe Journal of experimental medicine2011
The lineage-defining factors T-bet and Bcl-6 collaborate to regulate Th1 gene expression patterns.
Article in The Journal of experimental medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 1 of them a synthesis that pooled it.
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Who cites it
103 citing papers in PubMed, 1 synthesis or guideline pooled it, 151 citations in OpenAlex.
- T-bet: biological functions, molecular mechanisms, and therapeutic applications: a systematic review.Frontiers in immunology · 2026Pooled it
- Regulation of follicular helper T cell subset differentiation in health and disease.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Divergent phenotypic and functional roles of human T follicular helper cells from infancy to adulthood.bioRxiv : the preprint server for biology · 2026Article
- Divergent cytokine and transcriptional signatures control functional T follicular helper cell heterogeneity.Nature immunology · 2025Article
- Coordinated Regulation of Extrafollicular B Cell Responses by IL-12 and IFNγ.Immunological reviews · 2025Review
- Increased age-associated B cells in patients with acquired aplastic anemia correlate with IFN-γ.Blood advances · 2024Article
- Key Functions of the Transcription Factor BCL6 During T-Cell Differentiation.Advances in experimental medicine and biology · 2024Review
- Exploring TCR-like CAR-Engineered Lymphocyte Cytotoxicity against MAGE-A4.International journal of molecular sciences · 2023Article
- Vaccine adjuvant-elicited CD8Cell reports · 2023Article
- Immunotherapy targeting different immune compartments in combination with radiation therapy induces regression of resistant tumors.Nature communications · 2023Article
- Inhibitory IL-10-producing CD4eLife · 2023Article
- Aiolos represses CD4Nature communications · 2023Article
- TCF-1 Is Required for CD4 T Cell Persistence Functions during AlloImmunity.International journal of molecular sciences · 2023Article
- The TH1 cell lineage-determining transcription factor T-bet suppresses TH2 gene expression by redistributing GATA3 away from TH2 genes.Nucleic acids research · 2022Article
- Potential Role of CXCL13/CXCR5 Signaling in Immune Checkpoint Inhibitor Treatment in Cancer.Cancers · 2022Review
- Making memories with Bcl-6.The Journal of experimental medicine · 2022Article
- IFN-γ promotes the development of systemic lupus erythematosus through the IFNGR1/2-PSTAT1-TBX21 signaling axis.American journal of translational research · 2022Article
- CD4Cold Spring Harbor perspectives in biology · 2021Review
- Review
- Protein Immunization Induces Memory CD4Journal of immunology (Baltimore, Md. : 1950) · 2021Article
43 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The T-box transcription factor T-bet is important for the differentiation of naive CD4(+) T helper cells (Th cells) into the Th1 phenotype. Much is known about T-bet's role as a transcriptional activator, but less is known about the mechanisms by which T-bet functionally represses alternative Th cell genetic programs. In this study, we first identify Socs1, Socs3, and Tcf7 (TCF-1) as gene targets that are negatively regulated by T-bet. Significantly, T-bet's role in the repression of these genes is through a direct interaction with their promoters. Consistent with this, we identified two T-bet DNA-binding elements in the Socs1 promoter that are functionally used to down-regulate transcription in primary Th1 cells. Importantly, T-bet's novel role in transcriptional repression is because of its ability to physically associate with, and functionally recruit, the transcriptional repressor Bcl-6 to a subset of promoters. Furthermore, T-bet functionally recruits Bcl-6 to the Ifng locus in late stages of Th1 differentiation to repress its activity, possibly to prevent the overproduction of IFN-γ, which could result in autoimmunity. Collectively, these data establish a novel mechanism for T-bet-mediated gene repression in which two lineage-defining transcription factors, one a classical activator and one a repressor, collaborate to promote and properly regulate Th1 development.
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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.