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Blood, 15 March 2005, Vol. 105, No. 6, pp. 2495-2503. Prepublished online as a Blood First Edition Paper on November 23, 2004; DOI 10.1182/blood-2004-09-3644. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-09-3644v1 105/6/2495    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 Oppezzo, P. Articles by Vuillier, F. Search for Related Content PubMed PubMed Citation Articles by Oppezzo, P. Articles by Vuillier, F. Related Collections Immunobiology Neoplasia Gene Expression Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Different isoforms of BSAP regulate expression of AID in normal and chronic lymphocytic leukemia B cells Pablo Oppezzo, Gérard Dumas, Ana Inés Lalanne, Béatrice Payelle-Brogard, Christian Magnac, Otto Pritsch, Guillaume Dighiero, and Françoise Vuillier From the Unité d'Immuno-hématologie et d'Immunopathologie, Institut Pasteur, Paris, France, and Departamento de Bioquímica, Facultad de Medicina de Montevideo, Uruguay. Activation-induced cytidine deaminase (AID) is key to initiating somatic hypermutation (SHM) and class switch recombination (CSR), but its mode of action and regulation remains unclear. Since Pax-5 and Id-2 transcription factors play an opposing role in AID regulation, we have studied the expression of Pax-5, Id-2, and prdm-1 genes in 54 chronic lymphocytic leukemia (CLL) B cells. In 21 cases, presence of AID is constantly associated with high expression of the complete form of the Pax-5 gene (Pax-5a) and lower expression of the Id-2 and prdm-1 transcripts. In 33 cases, the absence of AID expression and CSR is associated with a reduction of Pax-5a and the appearance of a spliced form with a deletion in exon 8 (Pax-5/-Ex8). Stimulation with CD40L+interleukin 4 (IL-4) induces CSR, the presence of AID transcripts, up-regulation of Pax-5a and down-regulation of Pax-5/-Ex8, and Id-2 and prdm-1 transcripts. Pax-5a and Pax-5/-Ex8 are translated into 2 isoforms of the B-cell–specific activator protein (BSAP) and both are able to bind the AID-promoter region. Overall, these results suggest that Pax-5/-Ex8 could play an important role in the control of its own transcription and indirectly in AID expression and CSR. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: G. A. Robichaud, J.-P. Perreault, and R. J. Ouellette Development of an isoform-specific gene suppression system: the study of the human Pax-5B transcriptional element Nucleic Acids Res., July 10, 2008; (2008) gkn432v1. [Abstract] [Full Text] [PDF]

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