Tumors require a constant influx of myelomonocytic cells to support the angiogenesis and stroma remodeling needed for their growth. This is mediated by tumor-derived factors, which cause sustained myelopoiesis and the accumulation and functional differentiation of myelomonocytic cells, most of which are macrophages, at the tumor site. An important side effect of the accumulation and functional differentiation of these cells is that they can induce lymphocyte dysfunction. A complete understanding of the complex interplay between neoplastic and myelomonocytic cells might offer novel targets for therapeutic intervention aimed at depriving tumor cells of important growth support and enhancing the antitumor immune response.
Antonio Sica, Vincenzo Bronte
Title and authors | Publication | Year |
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Microbial translocation augments the function of adoptively transferred self/tumor-specific CD8+ T cells via toll-like receptor 4 signaling
Chrystal M. Paulos, Claudia Wrzesinski, Andrew Kaiser, Christian S. Hinrichs, Marcello Chieppa, Lydie Cassard, Douglas C. Palmer, Andrea Boni, Pawel Muranski, Zhiya Yu, Luca Gattinoni, Paul A. Antony, Steven A. Rosenberg, and Nicholas P. Restifo |
Journal of Clinical Investigation | 2007 |
Series overview: Harnessing the immune system to treat cancer
Nina Bhardwaj |
Journal of Clinical Investigation | 2007 |
Toll-like receptors in tumor immunotherapy
CM Paulos, A Kaiser, C Wrzesinski, CS Hinrichs, L Cassard, A Boni, P Muranski, L Sanchez-Perez, DC Palmer, Z Yu, PA Antony, L Gattinoni, SA Rosenberg, NP Restifo |
Clinical cancer research | 2007 |