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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. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-01-0027v1 105/3/1135    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 Wang, H. Articles by Sotomayor, E. M. Search for Related Content PubMed PubMed Citation Articles by Wang, H. Articles by Sotomayor, E. M. Related Collections Immunobiology Oncogenes and Tumor Suppressors Immunotherapy Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  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. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: H. Tanaka, H. Matsushima, A. Nishibu, B. E. Clausen, and A. 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