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Related Concept Videos

Histone Modification02:32

Histone Modification

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The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
Acetylation
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Histone variants are the histone proteins with structural and sequence variations. These variants may be regarded as “mutant” forms that replace their canonical histone counterparts in the nucleosomes. Specific post-translational modifications on the histone variants enable further chromatin complexity and regulate tissue-specific gene expression. The most common histone variants are from histone H2A, H2B, and linker histone H1 families. However, several variants of histone H3...
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Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...
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T Cell Types and Functions01:24

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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Proteins can undergo many types of post-translational modifications, often in response to changes in their environment. These modifications play an important role in the function and stability of these proteins. Covalently linked molecules include functional groups, such as methyl, acetyl, and phosphate groups, and also small proteins, such as ubiquitin. There are around 200 different types of covalent regulators that have been identified.
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Histone deacetylase function in CD4+ T cells.

Wilfried Ellmeier1, Christian Seiser2

  • 1Division of Immunobiology, Institute of Immunology, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria. wilfried.ellmeier@meduniwien.ac.at.

Nature Reviews. Immunology
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Histone deacetylases (HDACs) regulate T helper cell immunity and non-histone protein acetylation. HDAC inhibitors show promise for treating T cell-mediated immune diseases, with potential for broader applications.

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Area of Science:

  • Immunology
  • Epigenetics
  • Molecular Biology

Background:

  • T helper cell differentiation involves gene expression changes regulated by epigenetic processes.
  • Histone deacetylases (HDACs) and histone acetyltransferases (HATs) are key epigenetic regulators.
  • Acetylation of non-histone proteins by HDACs influences their function beyond gene expression.

Purpose of the Study:

  • To review the role of HDACs in CD4+ T cell-mediated immunity.
  • To highlight HDACs as potential therapeutic targets for T cell-mediated immune diseases.
  • To explore future research directions for isoform-selective HDAC inhibitors.

Main Methods:

  • Review of existing studies on HDACs in T cell immunity.
  • Analysis of epigenetic regulation mechanisms.
  • Discussion of clinical applications and future research.

Main Results:

  • HDACs are critical regulators of CD4+ T cell function in mice and humans.
  • HDACs are implicated in the pathogenesis of T cell-mediated immune diseases.
  • Isoform-selective HDAC inhibitors may offer expanded therapeutic potential.

Conclusions:

  • HDACs play a significant role in adaptive immunity.
  • Targeting HDACs presents a promising strategy for immune disease treatment.
  • Further research into isoform-specific HDAC inhibition is warranted for clinical advancement.