ArticleProceedings of the National Academy of Sciences of the United States of America2007
FOXP3 interactions with histone acetyltransferase and class II histone deacetylases are required for repression.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 223 papers.
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Who cites it
223 citing papers in PubMed, 398 citations in OpenAlex.
- Fli1 represses transcription of the human α2(I) collagen gene by recruitment of the HDAC1/p300 complex.PloS one · 2013Trial
- Multimerizing transcription factors FOXP3 and AIRE as chromatin architectural regulators.Nature immunology · 2026Review
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- Succinate drives gut inflammation by promoting FOXP3 degradation through a molecular switch.Nature immunology · 2025Article
- ACC1 is a dual metabolic-epigenetic regulator of Treg stability and immune tolerance.Molecular metabolism · 2025Article
- Regulatory T Cell Metabolism: A Promising Therapeutic Target for Cancer Treatment?Immune network · 2025Review
- Interferon-β and interleukin-6 exert opposing effects on Foxp3 acetylation to control regulatory T cell induction.Frontiers in immunology · 2025Article
- An integrated transcription factor framework for Treg identity and diversity.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Class IIa HDAC4 and HDAC7 cooperatively regulate gene transcription in Th17 cell differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Elusive modes of Foxp3 activity in versatile regulatory T cells.Frontiers in immunology · 2024Review
- T-regulatory cells require Sin3a for stable expression of Foxp3.Frontiers in immunology · 2024Article
- Reprogramming of regulatory T cells in inflammatory tumor microenvironment: can it become immunotherapy turning point?Frontiers in immunology · 2024Review
- Epigenetic regulation of human FOXP3+ Tregs: from homeostasis maintenance to pathogen defense.Frontiers in immunology · 2024Review
- Small-molecule TIP60 inhibitors enhance regulatory T cell induction through TIP60-P300 acetylation crosstalk.iScience · 2023Article
- Article
- Mutations from patients with IPEX ported to mice reveal different patterns of FoxP3 and Treg dysfunction.Cell reports · 2023Article
- Deacetylation of FOXP1 by HDAC7 potentiates self-renewal of mesenchymal stem cells.Stem cell research & therapy · 2023Article
- Histone deacetylase 7: a signalling hub controlling development, inflammation, metabolism and disease.The FEBS journal · 2023Review
163 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The forkhead family protein FOXP3 acts as a repressor of transcription and is both an essential and sufficient regulator of the development and function of regulatory T cells. The molecular mechanism by which FOXP3-mediated transcriptional repression occurs remains unclear. Here, we report that transcriptional repression by FOXP3 involves a histone acetyltransferase-deacetylase complex that includes histone acetyltransferase TIP60 (Tat-interactive protein, 60 kDa) and class II histone deacetylases HDAC7 and HDAC9. The N-terminal 106-190 aa of FOXP3 are required for TIP60-FOXP3, HDAC7-FOXP3 association, as well as for the transcriptional repression of FOXP3 via its forkhead domain. FOXP3 can be acetylated in primary human regulatory T cells, and TIP60 promotes FOXP3 acetylation in vivo. Overexpression of TIP60 but not its histone acetyltransferase-deficient mutant promotes, whereas knockdown of endogenous TIP60 relieved, FOXP3-mediated transcriptional repression. A minimum FOXP3 ensemble containing native TIP60 and HDAC7 is necessary for IL-2 production regulation in T cells. Moreover, FOXP3 association with HDAC9 is antagonized by T cell stimulation and can be restored by the protein deacetylation inhibitor trichostatin A, indicating a complex dynamic aspect of T suppressor cell regulation. These findings identify a previously uncharacterized complex-based mechanism by which FOXP3 actively mediates transcriptional repression.
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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.