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Blood, 1 November 2004, Vol. 104, No. 9, pp. 2849-2857. Prepublished online as a Blood First Edition Paper on July 8, 2004; DOI 10.1182/blood-2004-03-0790. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-03-0790v1 104/9/2849    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 van der Stoep, N. Articles by van den Elsen, P. J. Search for Related Content PubMed PubMed Citation Articles by van der Stoep, N. Articles by van den Elsen, P. J. Related Collections Immunobiology Signal Transduction Gene Expression Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY E47, IRF-4, and PU.1 synergize to induce B-cell-specific activation of the class II transactivator promoter III (CIITA-PIII) Nienke van der Stoep, Edwin Quinten, Marisa Marcondes Rezende, and Peter J. van den Elsen From the Department of Immunohematology and Blood Transfusion, Leiden University Medical Center (LUMC), Leiden, the Netherlands. In B cells, expression of CIITA and resulting major histocompatibility complex II (MHCII) is mediated exclusively by promoter III (CIITA-PIII) activation. Recent studies have established that CIITA-PIII also participates in the expression of CIITA in activated human T cells, dendritic cells, and monocytes. In this study we characterized the various regulatory elements and interacting factors of CIITA-PIII that account for specific activation in B lymphocytes. We identified 2 E-box motifs and an Ets/ISRE-consensus element (EICE) in CIITA-PIII as playing a crucial role in the B-cell-specific transcriptional regulation of CIITA. Abolishment of factor binding to these elements resulted in a strong reduction of CIITA-PIII activation in B cells only, whereas it did scarcely affect or not affect the activity of CIITA-PIII in activated T cells and monocytes. We show that in B cells, E47 and PU.1/IRF-4 interact with the E-box motifs and the EICE, respectively, and act synergistically in the activation of CIITA-PIII. Moreover, functional inhibition of either E47 or IRF-4 resulted in strong reduction of CIITA-PIII activity in B lymphocytes only. The finding that PU.1, IRF-4, and E47 play an important role in the B-cell-mediated activation of CIITA-PIII provides a link between antigen presentation functions and activation and differentiation events in B lymphocytes. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. Ito, C. Nishiyama, N. Nakano, M. Nishiyama, Y. Usui, K. Takeda, S. Kanada, K. Fukuyama, H. Akiba, T. Tokura, et al. Roles of PU.1 in monocyte- and mast cell-specific gene regulation: PU.1 transactivates CIITA pIV in cooperation with IFN-{gamma} Int. Immunol., July 1, 2009; 21(7): 803 - 816. [Abstract] [Full Text] [PDF] A. L. Shaffer, N.C. T. Emre, P. B. Romesser, and L. M. Staudt IRF4: Immunity. Malignancy! Therapy? Clin. Cancer Res., May 1, 2009; 15(9): 2954 - 2961. [Abstract] [Full Text] [PDF] D. Li, L. Qian, C. Chen, M. Shi, M. Yu, M. Hu, L. Song, B. Shen, and N. Guo Down-Regulation of MHC Class II Expression through Inhibition of CIITA Transcription by Lytic Transactivator Zta during Epstein-Barr Virus Reactivation J. Immunol., February 15, 2009; 182(4): 1799 - 1809. [Abstract] [Full Text] [PDF] M. R. Green, H. Yoon, and J. M. Boss Epigenetic Regulation during B Cell Differentiation Controls CIITA Promoter Accessibility J. 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