ArticleJournal of immunology (Baltimore, Md. : 1950)2016
HDAC3 Is Required for the Downregulation of RORγt during Thymocyte Positive Selection.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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
20 citing papers in PubMed, 32 citations in OpenAlex.
- HDAC3 inhibitors induce drug resistance by promoting IL-17 A production by T cells.Scientific reports · 2024Article
- Article
- Role of Histone Deacetylases in T-Cell Development and Function.International journal of molecular sciences · 2022Review
- Article
- Role of Epigenetics in the Regulation of Immune Functions of the Skin.The Journal of investigative dermatology · 2021Review
- Remodeling the chromatin landscape in T lymphocytes by a division of labor among transcription factors.Immunological reviews · 2021Review
- Hdac3 is an epigenetic inhibitor of the cytotoxicity program in CD8 T cells.The Journal of experimental medicine · 2020Article
- Role of HDACs in normal and malignant hematopoiesis.Molecular cancer · 2020Review
- Recent Update of HDAC Inhibitors in Lymphoma.Frontiers in cell and developmental biology · 2020Review
- Histone deacetylase 3 controls a transcriptional network required for B cell maturation.Nucleic acids research · 2019Article
- The Interaction between NKAP and HDAC3 Is Critical for T Cell Maturation.ImmunoHorizons · 2019Article
- Cutting Edge: HDAC3 Protects Double-Positive Thymocytes from P2X7 Receptor-Induced Cell Death.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Integrative regulation of physiology by histone deacetylase 3.Nature reviews. Molecular cell biology · 2019Review
- Article
- Restoring T Cell Tolerance, Exploring the Potential of Histone Deacetylase Inhibitors for the Treatment of Juvenile Idiopathic Arthritis.Frontiers in immunology · 2019Review
- Histone deacetylase function in CD4Nature reviews. Immunology · 2018Review
- Reduced Activity of HDAC3 and Increased Acetylation of Histones H3 in Peripheral Blood Mononuclear Cells of Patients with Rheumatoid Arthritis.Journal of immunology research · 2018Article
- The corepressor NCOR1 regulates the survival of single-positive thymocytes.Scientific reports · 2017Article
- Isoform-selective inhibitor of histone deacetylase 3 (HDAC3) limits pancreatic islet infiltration and protects female nonobese diabetic mice from diabetes.The Journal of biological chemistry · 2017Article
- Histone deacetylase 3 is required for iNKT cell development.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
To generate functional peripheral T cells, proper gene regulation during T cell development is critical. In this study, we found that histone deacetylase (HDAC) 3 is required for T cell development. T cell development in CD2-icre HDAC3 conditional knockout (cKO) mice (HDAC3-cKO) was blocked at positive selection, resulting in few CD4 and CD8 T cells, and it could not be rescued by a TCR transgene. These single-positive thymocytes failed to upregulate Bcl-2, leading to increased apoptosis. HDAC3-cKO mice failed to downregulate retinoic acid-related orphan receptor (ROR) γt during positive selection, similar to the block in positive selection in RORγt transgenic mice. In the absence of HDAC3, the RORC promoter was hyperacetylated. In the periphery, the few CD4 T cells present were skewed toward RORγt(+) IL-17-producing Th17 cells, leading to inflammatory bowel disease. Positive selection of CD8 single-positive thymocytes was restored in RORγt-KO Bcl-xL transgenic HDAC3-cKO mice, demonstrating that HDAC3 is required at positive selection to downregulate RORγt.
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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.