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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.
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Submitted December 10, 2007
Accepted February 6, 2008
Development and dynamics of robust T cell responses to CML under imatinib treatment
Christiane I-U. Chen, Holden T. Maecker, and Peter P. Lee*
Department of Medicine, Division of Hematology, Stanford University School of Medicine, Stanford, CA, United States
BD Biosciences - Immunocytometry Systems, San Jose, CA, United States
* Corresponding author; email: ppl{at}stanford.edu.
Novel molecular targeted therapies, such as imatinib for 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 anti-leukemia immune responses in an antigen unbiased way, we utilized cryopreserved autologous pre-treatment blood samples (representing predominantly leukemic cells) as stimulators to detect anti-leukemia 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 anti-leukemia T cell responses develop in the majority of CML patients (9/14) in remission, and that CD4+ T cells producing TNF- (median 17.6%) represent the major response over IFN- . 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.
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