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  • Histone deacetylase inhibitors and transplantation
  • Tao R; de Zoeten EF; Ozkaynak E; Wang L; Li B; Greene MI; Wells AD; Hancock WW
  • Curr Opin Immunol 2007[Oct]; 19 (5): 589-95
  • Simply detecting the presence or absence of Foxp3, a transcription factor characteristic of naturally occurring CD4+ CD25+ regulatory T cells (Tregs), now appears of minimal value in predicting the outcome of immunologic responses, since dividing human CD4+ effector T cells can induce Foxp3 without attaining repressive functions, and additional molecular interactions, as well epigenetic events, affect Foxp3-dependent Treg functions in humans and mice. Experimentally, in vivo and in vitro studies show histone deacetylase inhibitors (HDACi) can enhance the numbers and suppressive function of regulatory T cells (Tregs) by promoting Foxp3+ cell production, enhancing chromatin remodeling within Tregs, and inducing acetylation of Foxp3 protein itself. Human studies consistent with a role for HDACi in controlling Fox3-dependent Treg functions are also available. We review these molecular interactions and how they may be exploited therapeutically to enhance Treg-dependent functions, including post-transplantation.
  • |*Histone Deacetylase Inhibitors[MESH]
  • |*Transplantation Immunology[MESH]
  • |Animals[MESH]
  • |Epigenesis, Genetic[MESH]
  • |Forkhead Transcription Factors/genetics/*metabolism[MESH]
  • |Histone Deacetylases/*metabolism[MESH]
  • |Humans[MESH]
  • |T-Lymphocytes, Regulatory/*immunology/metabolism[MESH]

  • *{{pmid17719760}}
    *<b>[ Histone deacetylase inhibitors and transplantation ]</b> Curr Opin Immunol 2007; 19(5) ; 589-95 Tao R; de Zoeten EF; Ozkaynak E; Wang L; Li B; Greene MI; Wells AD; Hancock WW


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    Curr Opin Immunol

    589 5.19 2007