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Blood, 1 June 2008, Vol. 111, No. 11, pp. 5342-5349. Prepublished online as a Blood First Edition Paper on March 7, 2008; DOI 10.1182/blood-2007-12-128397. This Article Full Text Full Text (PDF) Supplemental Figure All Versions of this Article: blood-2007-12-128397v1 111/11/5342    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 Chen, C. I-U. Articles by Lee, P. P. Search for Related Content PubMed PubMed Citation Articles by Chen, C. I-U. Articles by Lee, P. P. Related Collections Immunobiology Neoplasia Signal Transduction Free Research Articles Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Development and dynamics of robust T-cell responses to CML under imatinib treatment Christiane I-U. Chen1, Holden T. Maecker2, and Peter P. Lee2 1 Department of Medicine, Division of Hematology, Stanford University School of Medicine, Stanford, CA; and 2 BD Biosciences–Immunocytometry Systems, San Jose, CA Novel molecular targeted therapies, such as imatinib for chronic myelogenous leukemia (CML), represent the first agents that inhibit cancer cells more than other dividing cells, such as immune cells. We hypothesize that imatinib may create a window in which the immune response is partially restored while apoptotic leukemic cells are present, thus rendering leukemic cells immunogenic as patients enter remission. To detect and quantify antileukemia immune responses in an antigen-unbiased way, we used cryopreserved autologous pretreatment blood samples (representing predominantly leukemic cells) as stimulators to detect antileukemia T-cell responses in CML patients in remission on imatinib. We studied patients over time to address the dynamics of such responses. Our data show that antileukemia T-cell responses develop in the majority of CML patients (9 of 14) in remission and that CD4+ T cells producing tumor necrosis factor- (median 17.6%) represent the major response over interferon-. This confirms the immune system's ability to respond to leukemia under certain conditions. Such responses may be further amplified as a potential therapy that synergizes with imatinib for improved control of CML. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. Louvet, G. L. Szot, J. Lang, M. R. Lee, N. Martinier, G. Bollag, S. Zhu, A. Weiss, and J. A. Bluestone Tyrosine kinase inhibitors reverse type 1 diabetes in nonobese diabetic mice PNAS, December 2, 2008; 105(48): 18895 - 18900. [Abstract] [Full Text] [PDF] N. Larmonier, N. Janikashvili, C. J. LaCasse, C. B. Larmonier, J. Cantrell, E. Situ, T. Lundeen, B. Bonnotte, and E. Katsanis Imatinib Mesylate Inhibits CD4+CD25+ Regulatory T Cell Activity and Enhances Active Immunotherapy against BCR-ABL- Tumors J. Immunol., November 15, 2008; 181(10): 6955 - 6963. [Abstract] [Full Text] [PDF]

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