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Prepublished online as a Blood First Edition Paper on January 9, 2003; DOI 10.1182/blood-2002-10-3175. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-10-3175v1 101/10/4029    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 Dighiero, G. Search for Related Content PubMed PubMed Citation Articles by Oppezzo, P. Articles by Dighiero, G. Related Collections Immunobiology Neoplasia Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 May 2003, Vol. 101, No. 10, pp. 4029-4032 IMMUNOBIOLOGY Brief report Chronic lymphocytic leukemia B cells expressing AID display dissociation between class switch recombination and somatic hypermutation Pablo Oppezzo, Françoise Vuillier, Yuri Vasconcelos, Gérard Dumas, Christian Magnac, Béatrice Payelle-Brogard, Otto Pritsch, and Guillaume Dighiero From the Unité d'Immuno-hématologie et d'Immunopathologie, Institut Pasteur, Paris, France; Disciplina de Hematologia e Hemoterapia, Universidade Federal de Sao Paulo, Brazil; and Departamento de Bioquímica, Facultad de Medicina de Montevideo, Uruguay. In B cells, somatic hypermutation (SHM) and class switch recombination (CSR) depend on the activation-induced cytidine deaminase (AID) gene product, although the precise mode of action of AID remains unknown. Because some chronic lymphocytic leukemia (CLL) B cells can undergo CSR without SHM, it constitutes a useful model to dissect AID function. In this work, we have studied AID expression, the presence of mutations in the preswitch µ DNA region, CSR, and the SHM in 65 CLL patients. Our results demonstrate that unmutated CLL B cells can constitutively express AID and that AID expression is associated with the presence of mutations in the preswitch region and in clonally related isotype-switched transcripts. They also demonstrate that in CLL without constitutive AID expression, AID induction on stimulation results in preswitch mutations and the CSR process. Our results show a dissociation between SHM and CSR in CLL and suggest that, in this disease, AID would require additional help for carrying out the SHM process. © 2003 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? 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