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Blood, 15 January 2004, Vol. 103, No. 2, pp. 538-544. Prepublished online as a Blood First Edition Paper on September 22, 2003; DOI 10.1182/blood-2003-03-0975. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-03-0975v1 103/2/538    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 Appel, S. Articles by Brossart, P. Search for Related Content PubMed PubMed Citation Articles by Appel, S. Articles by Brossart, P. Related Collections Hematopoiesis and Stem Cells Immunobiology Oncogenes and Tumor Suppressors Related Letter in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS Imatinib mesylate affects the development and function of dendritic cells generated from CD34+ peripheral blood progenitor cells Silke Appel, Andreas M. Boehmler, Frank Grünebach, Martin R. Müller, Anette Rupf, Markus M. Weck, Ulrike Hartmann, Volker L. Reichardt, Lothar Kanz, Tim H. Brümmendorf, and Peter Brossart From the Department of Hematology, Oncology, and Immunology, University of Tübingen, Tübingen, Germany. Imatinib mesylate (STI571) is a competitive Bcr-Abl tyrosine kinase inhibitor and has yielded encouraging results in treatment of chronic myelogenous leukemia (CML) and gastrointestinal stroma tumors (GISTs). Apart from inhibition of the Abl protein tyrosine kinases, it also shows activity against platelet-derived growth factor receptor (PDGF-R), c-Kit, Abl-related gene (ARG), and their fusion proteins while sparing other kinases. In vitro studies have revealed that imatinib mesylate can inhibit growth of cell lines and primitive malignant progenitor cells in CML expressing Bcr-Abl. However, little is known about the effects of imatinib mesylate on nonmalignant hematopoietic cells. In the current study we demonstrate that in vitro exposure of mobilized human CD34+ progenitors to therapeutic concentrations of imatinib mesylate (1-5 µM) inhibits their differentiation into dendritic cells (DCs). DCs obtained after 10 to 16 days of culture in the presence of imatinib mesylate showed concentration-dependent reduced expression levels of CD1a and costimulatory molecules such as CD80 and CD40. Furthermore, exposure to imatinib mesylate inhibited the induction of primary cytotoxic T-lymphocyte (CTL) responses. The inhibitory effects of imatinib mesylate were accompanied by down-regulation of nuclear localized RelB protein. Our results demonstrate that imatinib mesylate can act on normal hematopoietic cells and inhibits the differentiation and function of DCs, which is in part mediated via the nuclear factor B signal transduction pathway. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Letter in Blood Online: Imatinib mesylate impairs Flt3L-mediated dendritic cell expansion and antitumor effects in vivo Julien Taïeb, Koji Maruyama, Christophe Borg, Magali Terme, Laurence Zitvogel, Silke Appel, and Peter Brossart Blood 2004 103: 1966-1967. [Full Text] [PDF] This article has been cited by other articles: M. M. Hipp, N. Hilf, S. Walter, D. Werth, K. M. Brauer, M. P. Radsak, T. Weinschenk, H. Singh-Jasuja, and P. 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