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Blood, 1 April 2007, Vol. 109, No. 7, pp. 2878-2886. Prepublished online as a Blood First Edition Paper on December 5, 2006; DOI 10.1182/blood-2006-07-037754. This Article Full Text (PDF) All Versions of this Article: blood-2006-07-037754v1 109/7/2878    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Bandyopadhyay, S. Articles by Macian, F. Search for Related Content PubMed PubMed Citation Articles by Bandyopadhyay, S. Articles by Macian, F. Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted July 26, 2006 Accepted November 22, 2006 Interleukin 2 gene transcription is regulated by Ikaros-induced changes in histone acetylation in anergic T cells Sanmay Bandyopadhyay, Myrianne Dure, Monika Paroder, Noemi Soto-Nieves, Irene Puga, and Fernando Macian* Dept of Pathology, Albert Einstein College of Medicine, Bronx, NY, United States * Corresponding author; email: fmacianj{at}aecom.yu.edu. In T cells anergy may be evoked by an unbalanced stimulation of the T cell receptor in the absence of costimulation. Anergic T cells are unresponsive to new antigen receptor engagement and do not produce interleukin 2. We present evidence that anergizing stimuli induce changes in histone acetylation, which mediate transcriptional repression of interleukin 2 expression. In response to calcium signaling, anergic T cells upregulate the expression of Ikaros, a zinc finger transcription factor essential for lymphoid lineage determination. Ikaros binds to the interleukin 2 promoter where it induces histone deacetylation. Confirming the role of Ikaros in the induction of T cell anergy, cells with reduced Ikaros activity show defective inactivation in response to an anergizing stimulus. We propose a model in which tolerizing stimuli induce epigenetic changes on the interleukin 2 locus that are responsible for the stable inhibition of the expression of this cytokine in anergic T cells. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Bringing IL-2 down to earth Jonathan D. Powell Blood 2007 109: 2671-2672. [Full Text] [PDF] This article has been cited by other articles: S. E. Umetsu and S. Winandy Ikaros Is a Regulator of Il10 Expression in CD4+ T Cells J. Immunol., November 1, 2009; 183(9): 5518 - 5525. [Abstract] [Full Text] [PDF] A. Nayak, J. Glockner-Pagel, M. Vaeth, J. E. Schumann, M. Buttmann, T. Bopp, E. Schmitt, E. Serfling, and F. Berberich-Siebelt Sumoylation of the Transcription Factor NFATc1 Leads to Its Subnuclear Relocalization and Interleukin-2 Repression by Histone Deacetylase J. Biol. Chem., April 17, 2009; 284(16): 10935 - 10946. [Abstract] [Full Text] [PDF] N. Soto-Nieves, I. Puga, B. T. Abe, S. Bandyopadhyay, I. Baine, A. Rao, and F. Macian Transcriptional complexes formed by NFAT dimers regulate the induction of T cell tolerance J. Exp. Med., April 13, 2009; 206(4): 867 - 876. [Abstract] [Full Text] [PDF]

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