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Blood, 1 April 2006, Vol. 107, No. 7, pp. 2871-2878. Prepublished online as a Blood First Edition Paper on December 8, 2005; DOI 10.1182/blood-2005-07-3014. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-07-3014v1 107/7/2871    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 Horna, P. Articles by Sotomayor, E. M. Search for Related Content PubMed PubMed Citation Articles by Horna, P. Articles by Sotomayor, E. M. Related Collections Immunobiology Neoplasia Immunotherapy Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY In vivo disruption of tolerogenic cross-presentation mechanisms uncovers an effective T-cell activation by B-cell lymphomas leading to antitumor immunity Pedro Horna, Alex Cuenca, Fengdong Cheng, Jason Brayer, Hong-Wei Wang, Ivan Borrello, Hyam Levitsky, and Eduardo M. Sotomayor From the Department of Interdisciplinary Oncology, H. Lee Moffitt Cancer Center and Research Institute, University of South Florida, Tampa, FL; and the Sidney Kimmel Cancer Center, Johns Hopkins University, Baltimore, MD. Bone marrow-derived antigen-presenting cells (APCs) play a central role in the induction of tolerance to tumor antigens expressed by B-cell lymphomas. Here we show that in vivo disruption of this APC-mediated tolerogenic mechanism unveils an intrinsic ability of malignant B cells to efficiently present tumor antigens to antigen-specific CD4+ T cells, resulting in a strong antitumor effect. This intrinsic antigen-presenting ability of malignant B cells is, however, overridden by tolerogenic bone marrow-derived APCs, leading instead to T-cell unresponsiveness and lack of antitumor effect. These results highlight the concept that therapeutic strategies aimed at enhancing the antigen-presenting function of B-cell lymphomas might not succeed unless the tolerogenic mechanisms mediated by bone marrow-derived APCs are disrupted in the first place. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: P. Serafini, S. Mgebroff, K. Noonan, and I. Borrello Myeloid-Derived Suppressor Cells Promote Cross-Tolerance in B-Cell Lymphoma by Expanding Regulatory T Cells Cancer Res., July 1, 2008; 68(13): 5439 - 5449. [Abstract] [Full Text] [PDF] Z.-Z. Yang, A. J. Novak, S. C. Ziesmer, T. E. Witzig, and S. M. Ansell CD70+ non-Hodgkin lymphoma B cells induce Foxp3 expression and regulatory function in intratumoral CD4+CD25 T cells Blood, October 1, 2007; 110(7): 2537 - 2544. [Abstract] [Full Text] [PDF] Y. Chung, H. Qin, C.-Y. Kang, S. Kim, L. W. Kwak, and C. Dong An NKT-mediated autologous vaccine generates CD4 T-cell dependent potent antilymphoma immunity Blood, September 15, 2007; 110(6): 2013 - 2019. [Abstract] [Full Text] [PDF] R. R. French, V. Y. Taraban, G. R. Crowther, T. F. Rowley, J. C. Gray, P. W. Johnson, A. L. Tutt, A. Al-Shamkhani, and M. J. Glennie Eradication of lymphoma by CD8 T cells following anti-CD40 monoclonal antibody therapy is critically dependent on CD27 costimulation Blood, June 1, 2007; 109(11): 4810 - 4815. [Abstract] [Full Text] [PDF] Z.-Z. Yang, A. J. Novak, S. C. Ziesmer, T. E. Witzig, and S. M. Ansell Attenuation of CD8+ T-Cell Function by CD4+CD25+ Regulatory T Cells in B-Cell Non-Hodgkin's Lymphoma. Cancer Res., October 15, 2006; 66(20): 10145 - 10152. [Abstract] [Full Text] [PDF]

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