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Blood, 1 October 2007, Vol. 110, No. 7, pp. 2556-2560. Prepublished online as a Blood First Edition Paper on June 19, 2007; DOI 10.1182/blood-2007-01-071001. This Article Full Text (PDF) Supplemental Methods, Table, and Figure All Versions of this Article: blood-2007-01-071001v1 110/7/2556    most recent Alert me when this article is cited Alert me if a correction is posted 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 Scheich, F. Articles by Bernhard, H. Search for Related Content PubMed PubMed Citation Articles by Scheich, F. Articles by Bernhard, H. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted January 29, 2007 Accepted June 13, 2007 The immunogenicity of Bcr-Abl expressing dendritic cells is dependent on the Bcr-Abl kinase activity and dominated by Bcr-Abl regulated antigens Florian Scheich, Justus Duyster, Christian Peschel, and Helga Bernhard* Department of Hematology/Oncology, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany * Corresponding author; email: helga.bernhard{at}lrz.tum.de. In Ph+ chronic myeloid leukemia (CML), the constitutively active Bcr-Abl kinase leads to the upregulation and activation of multiple genes, which may subsequently result in the expression of leukemia-associated antigens. In this study, we investigated the immunogenicity of Bcr-Abl regulated antigens by stimulating CD8+ T lymphocytes with autologous dendritic cells transfected with RNA coding for Bcr-Abl wild type or a kinase deficient mutant. Significant HLA class I-restricted T-cell responses were detected against antigens regulated by the Bcr-Abl kinase, but not towards the Bcr-Abl protein itself. The T-cell repertoire of a patient with CML in major molecular remission due to imatinib mesylate was also dominated by T cells directed against Bcr-Abl regulated antigens. These results encourage the development of immunotherapeutical approaches against Bcr-Abl regulated antigens for the treatment of CML patients with residual disease following therapy with Bcr-Abl kinase inhibitors. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. I-U. Chen, H. T. Maecker, and P. P. Lee Development and dynamics of robust T-cell responses to CML under imatinib treatment Blood, June 1, 2008; 111(11): 5342 - 5349. [Abstract] [Full Text] [PDF]

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