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HDAC7 regulates apoptosis in developing thymocytes.

Eric Verdin1, Frank Dequiedt, Herb Kasler

  • 1Gladstone Institute of Virology and Immunology, Department of Medicine, University of California, San Francisco, PO Box 419100, San Francisco, CA 94141-9100, USA.

Novartis Foundation Symposium
|June 3, 2004
PubMed
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Histone deacetylase 7 (HDAC7) regulates T cell development in the thymus. HDAC7 controls apoptosis during T cell selection, crucial for establishing central immune tolerance and preventing autoimmunity.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Central immune tolerance in T cells is established in the thymus through positive and negative selection processes.
  • These selection processes involve interactions between thymocytes and antigen-presenting cells, crucial for eliminating self-reactive T cells.
  • Dysregulation of selection can lead to autoimmunity and loss of immune tolerance.

Purpose of the Study:

  • To investigate the role of histone deacetylase 7 (HDAC7) in T cell development and central immune tolerance.
  • To elucidate the molecular mechanism by which HDAC7 influences negative selection in thymocytes.

Main Methods:

  • Analysis of HDAC7 expression in CD4+CD8+ double-positive thymocytes.
  • Investigated the effect of HDAC7 on Nur77 expression, a key regulator of apoptosis.

Related Experiment Videos

  • Examined the role of the transcription factor MEF2D in mediating HDAC7's function.

    • Main Results:

    • HDAC7 is highly expressed in double-positive thymocytes and inhibits Nur77 expression via MEF2D.
    • T cell receptor activation leads to nuclear export of HDAC7, derepression of Nur77, and induction of apoptosis.
    • HDAC7 acts as a critical regulator of Nur77-mediated apoptosis during thymocyte development.

    Conclusions:

    • HDAC7 plays a significant role in regulating apoptosis during thymocyte selection.
    • HDAC7's function is essential for controlling Nur77 expression and maintaining central immune tolerance.
    • HDAC7 is a key molecular player in preventing the escape of self-reactive T cells.