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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.

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IMMUNOBIOLOGY

Brief Report

The immunogenicity of Bcr-Abl–expressing dendritic cells is dependent on the Bcr-Abl kinase activity and dominated by Bcr-Abl–regulated antigens

Florian Scheich1, Justus Duyster1, Christian Peschel1, and Helga Bernhard1

1 Department of Hematology/Oncology, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany

In Ph+ chronic myeloid leukemia (CML), the constitutively active Bcr-Abl kinase leads to the up-regulation 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 toward 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 immunotherapeutic approaches against Bcr-Abl–regulated antigens for the treatment of CML patients with residual disease following therapy with Bcr-Abl kinase inhibitors.


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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.
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