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Blood, 1 September 2008, Vol. 112, No. 5, pp. 1804-1812. Prepublished online as a Blood First Edition Paper on June 13, 2008; DOI 10.1182/blood-2008-01-136440. This Article Full Text Full Text (PDF) Supplemental Tables and Figures All Versions of this Article: blood-2008-01-136440v1 112/5/1804    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 Schmidlin, H. Articles by Blom, B. Search for Related Content PubMed PubMed Citation Articles by Schmidlin, H. Articles by Blom, B. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Spi-B inhibits human plasma cell differentiation by repressing BLIMP1 and XBP-1 expression Heike Schmidlin1, Sean A. Diehl1, Maho Nagasawa1, Ferenc A. Scheeren1, Remko Schotte1, Christel H. Uittenbogaart2, Hergen Spits1,3, and Bianca Blom1 1 Department of Cell Biology and Histology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; Departments of2 Microbiology, Immunology and Molecular Genetics, and Pediatrics, David Geffen School of Medicine at the University of California Los Angeles; and 3 Department of Immunology Discovery, Genentech, South San Francisco, CA The terminal differentiation of B cells into antibody-secreting plasma cells is tightly regulated by a complex network of transcription factors. Here we evaluated the role of the Ets factor Spi-B during terminal differentiation of human B cells. All mature tonsil and peripheral blood B-cell subsets expressed Spi-B, with the exception of plasma cells. Overexpression of Spi-B in CD19+ B cells inhibited, similar to the known inhibitor BCL-6, the expression of plasma cell–associated surface markers and transcription factors as well as immunoglobulin production, ie, in vitro plasma cell differentiation. The arrest in B-cell differentiation enforced by Spi-B was independent of the transactivation domain, but dependent on the Ets-domain. By chromatin immunoprecipitation and assays using an inducible Spi-B construct BLIMP1 and XBP-1 were identified as direct target genes of Spi-B mediated repression. We propose a novel role for Spi-B in maintenance of germinal center and memory B cells by direct repression of major plasma cell factors and thereby plasma cell differentiation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Middendorp, Y. Xiao, J.-Y. Song, V. Peperzak, P. H. L. Krijger, H. Jacobs, and J. Borst Mice deficient for CD137 ligand are predisposed to develop germinal center-derived B-cell lymphoma Blood, September 10, 2009; 114(11): 2280 - 2289. [Abstract] [Full Text] [PDF] J. Hauser, J. Verma-Gaur, A. Wallenius, and T. Grundstrom Initiation of Antigen Receptor-Dependent Differentiation into Plasma Cells by Calmodulin Inhibition of E2A J. Immunol., July 15, 2009; 183(2): 1179 - 1187. [Abstract] [Full Text] [PDF]

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