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Literature DB >> 19050254

T-bet dependent removal of Sin3A-histone deacetylase complexes at the Ifng locus drives Th1 differentiation.

Shaojing Chang¹, Patrick L Collins, Thomas M Aune.

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.

Entities: CellLine Chemical Disease Gene Species

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Year: 2008 PMID： 19050254 PMCID： PMC2794428 DOI： 10.4049/jimmunol.181.12.8372

Source DB: PubMed Journal: J Immunol ISSN： 0022-1767 Impact factor: 5.422

52 in total

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10. Essential role for interferon-gamma and interleukin-6 in autoimmune insulin-dependent diabetes in NOD/Wehi mice.

Authors: I L Campbell; T W Kay; L Oxbrow; L C Harrison
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22 in total

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2. Modular utilization of distal cis-regulatory elements controls Ifng gene expression in T cells activated by distinct stimuli.

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Review 3. The interface between transcriptional and epigenetic control of effector and memory CD8⁺ T-cell differentiation.

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T-bet dependent removal of Sin3A-histone deacetylase complexes at the Ifng locus drives Th1 differentiation.

Review 1. Unlocking the mechanisms of transcription factor YY1: are chromatin modifying enzymes the key?

2. T helper cell fate specified by kinase-mediated interaction of T-bet with GATA-3.

3. Inhibition of Th1 development mediated by GATA-3 through an IL-4-independent mechanism.

4. Requirement for Stat4 in interleukin-12-mediated responses of natural killer and T cells.

5. MeCP2 is a transcriptional repressor with abundant binding sites in genomic chromatin.

6. Activation of p53 sequence-specific DNA binding by acetylation of the p53 C-terminal domain.

7. Stat3 dimerization regulated by reversible acetylation of a single lysine residue.

8. A Hidden Markov Model approach to variation among sites in rate of evolution.

9. The nuclear factor YY1 suppresses the human gamma interferon promoter through two mechanisms: inhibition of AP1 binding and activation of a silencer element.

10. Essential role for interferon-gamma and interleukin-6 in autoimmune insulin-dependent diabetes in NOD/Wehi mice.

Review 1. Histone/protein deacetylases and T-cell immune responses.

2. Modular utilization of distal cis-regulatory elements controls Ifng gene expression in T cells activated by distinct stimuli.

Review 3. The interface between transcriptional and epigenetic control of effector and memory CD8⁺ T-cell differentiation.

Review 4. Transcriptional regulatory networks for CD4 T cell differentiation.

Review 5. Generating long-lived CD8(+) T-cell memory: Insights from epigenetic programs.

6. Osteoclast-Primed Foxp3+ CD8 T Cells Induce T-bet, Eomesodermin, and IFN-γ To Regulate Bone Resorption.

7. Distal regions of the human IFNG locus direct cell type-specific expression.

Review 8. Modulation of antigen-presenting cells by HDAC inhibitors: implications in autoimmunity and cancer.

Review 9. Inhibition of histone deacetylases in inflammatory bowel diseases.

10. Overexpression of methyl-CpG binding protein 2 impairs T(H)1 responses.