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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.
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Submitted July 27, 2005
Accepted November 28, 2005
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*
Department of Interdisciplinary Oncology, H. Lee Moffitt Cancer Center & Research Institute at the University of South Florida, Tampa, FL, USA
Sidney Kimmel Cancer Center, Johns Hopkins, Baltimore, MD, USA
* Corresponding author; email: sotomed{at}moffitt.usf.edu.
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 to enhance 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.
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