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Blood, 1 February 2005, Vol. 105, No. 3, pp. 1135-1143.
Prepublished online as a Blood First Edition Paper on September 28, 2004; DOI 10.1182/blood-2004-01-0027.
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IMMUNOBIOLOGY
Imatinib mesylate (STI-571) enhances antigen-presenting cell function and overcomes tumor-induced CD4+ T-cell tolerance
Hongwei Wang,
Fengdong Cheng,
Alex Cuenca,
Pedro Horna,
Zheng Zheng,
Kapil Bhalla, and
Eduardo M. Sotomayor
From the Department of Interdisciplinary Oncology, H. Lee Moffitt Cancer Center & Research Institute at the University of South Florida, Tampa, FL.
Tumor antigen–specific T-cell tolerance imposes a significant barrier to the development of effective therapeutic cancer vaccines. Bone marrow–derived antigen-presenting cells (APCs) are critical in the induction of this unresponsive state. Here we show that in vitro treatment of APCs with the tyrosine kinase inhibitor, imatinib mesylate (STI-571), enhances the activation of naive antigen-specific T cells and restores the responsiveness of tolerant T cells from tumor-bearing hosts. Furthermore, in vivo treatment with STI-571 not only prevented the induction of tolerance in tumor-specific CD4+ T cells, preserving their responsiveness to a subsequent immunization, but also resulted in enhanced vaccine efficacy. These findings demonstrate that tolerance to tumor antigens is not an insurmountable obstacle and points to modulation of APC function as a promising strategy in the immunotherapy of cancer.
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