ArticleJournal of immunology (Baltimore, Md. : 1950)2008
T-bet dependent removal of Sin3A-histone deacetylase complexes at the Ifng locus drives Th1 differentiation.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 50 citations in OpenAlex.
- Modulating effects of heat-killed and liveThe veterinary quarterly · 2024Article
- The Killer's Web: Interconnection between Inflammation, Epigenetics and Nutrition in Cancer.International journal of molecular sciences · 2024Review
- Current treatment strategies targeting histone deacetylase inhibitors in acute lymphocytic leukemia: a systematic review.Frontiers in oncology · 2024Review
- Histone deacetylase inhibitors: targeting epigenetic regulation in the treatment of acute leukemia.Therapeutic advances in hematology · 2024Review
- The Correlation Between IFNG Gene Methylation and Th1|Th2 Cell Balance in ROU and the Interventional Study of Jiaweidaochi Powder.Applied biochemistry and biotechnology · 2023Article
- Review
- T-helper cells flexibility: the possibility of reprogramming T cells fate.Frontiers in immunology · 2023Review
- The increasing hematopoietic effect of the combined treatment of Korean Red Ginseng andJournal of ginseng research · 2021Article
- Epigenetic Reprogramming of CD4Frontiers in immunology · 2021Review
- Tumor Burden and Immunotherapy: Impact on Immune Infiltration and Therapeutic Outcomes.Frontiers in immunology · 2020Review
- Juvenile idiopathic arthritis associated with a mutation in GATA3.Arthritis research & therapy · 2019Article
- Immunoepigenetics Combination Therapies: An Overview of the Role of HDACs in Cancer Immunotherapy.International journal of molecular sciences · 2019Review
- Therapeutic Cancer Vaccines-T Cell Responses and Epigenetic Modulation.Frontiers in immunology · 2018Review
- Epi-drugs in combination with immunotherapy: a new avenue to improve anticancer efficacy.Clinical epigenetics · 2017Review
- Nutrients and the microenvironment to feed a T cell army.Seminars in immunology · 2016Review
- Osteoclast-Primed Foxp3+ CD8 T Cells Induce T-bet, Eomesodermin, and IFN-γ To Regulate Bone Resorption.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Generating long-lived CD8(+) T-cell memory: Insights from epigenetic programs.European journal of immunology · 2016Review
- Combining HDAC inhibitors with oncolytic virotherapy for cancer therapy.Oncolytic virotherapy · 2015Review
- The interface between transcriptional and epigenetic control of effector and memory CD8⁺ T-cell differentiation.Immunological reviews · 2014Review
- Transcriptional regulatory networks for CD4 T cell differentiation.Current topics in microbiology and immunology · 2014Review
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 2 institutions in 1 country.
Funding
Abstract
Forming and removing epigenetic histone marks at gene loci are central processes in differentiation. Here, we explored mechanisms establishing long-range H4 acetylation marks at the Ifng locus during Th1 lineage commitment. In Th0 cells, histone deacetylase (HDAC)-Sin3A complexes recruited to the Ifng locus actively prevented accumulation of H4 acetylation marks. Th1 differentiation caused loss of HDAC-Sin3A complexes by T-bet-dependent mechanisms and accumulation of H4 acetylation marks. HDAC-Sin3A complexes were absent from the locus in NOD Th0 cells, obviating the need for Th1 differentiation signals to establish histone marks and Th1 differentiation. Thus, Ifng transcription is actively prevented in Th0 cells via epigenetic mechanisms and epigenetic defects allow unregulated Ifng transcription that may contribute to autoimmunity.
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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.