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The Journal of Immunology, 2006, 176: 5023-5032.
Copyright © 2006 by The American Association of Immunologists

Ovarian Cancer Cells Polarize Macrophages Toward A Tumor-Associated Phenotype1

Thorsten Hagemann2,3,*, Julia Wilson2,*, Frances Burke*, Hagen Kulbe*, Ninfeng Fiona Li*, Annette Plüddemann{dagger}, Kellie Charles*, Siamon Gordon{dagger} and Frances R. Balkwill*

* Cancer Research United Kingdom Translational Oncology Laboratory, Barts & The London, Queen Mary’s School of Medicine and Dentistry, Charterhouse Square, London, United Kingdom; and {dagger} Sir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom

Tumor-associated macrophages (TAM) may have tumor-promoting activity, but it is not clear how their phenotype is achieved. In this study, we demonstrate that ovarian cancer cells switch cocultured macrophages to a phenotype similar to that found in ovarian tumors. Tumor cells caused dynamic changes in macrophage cytokine, chemokine, and matrix metalloprotease mRNA, and protein-inducing mediators that are found in human cancer. Macrophage mannose, mannose receptor, and scavenger receptors (SR-As) were also up-regulated by coculture, but not by conditioned medium. To further validate the model, we studied SR-A regulation on TAM in vitro and in vivo. Coculture of murine macrophages from mice deficient in TNF-{alpha} or its receptors revealed that TNF-{alpha} was key to SR-A induction via its p75 receptor. SR-A expression was also reduced in TAM from ovarian cancers treated with anti-TNF-{alpha} Abs or grown in TNF-{alpha}–/– mice. Chemical communication between tumor cells and macrophages may be important in regulating the cancer cytokine microenvironment.




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