Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
4496398 | Journal of Theoretical Biology | 2013 | 12 Pages |
•PDE model of tumor growth.•Tumor associated macrophages.•The transition from M1 to M2 macrophages under influence of the cancer.•Role of CD200R in immunoediting.•IL-10 downregulation in M2 and IL-12 upregulation in M1.
CD200 is a cell membrane protein that interacts with CD200 receptor (CD200R) of myeloid lineage cells. During tumor initiation and progression, CD200-positive tumor cells can interact with M1 and M2 macrophages through CD200–CD200R-compex, and downregulate IL-10 and IL-12 productions secreted primarily by M2 and M1 macrophages, respectively. In the tumor microenvironment, IL-10 inhibits the activation of cytotoxic T lymphocytes (CTL), while IL-12 enhances CTL activation. In this paper, we used a system approach to determine the combined effect of CD200–CD200R interaction on tumor proliferation by developing a mathematical model. We demonstrate that blocking CD200 on tumor cells may have opposite effects on tumor proliferation depending on the “affinity” of the macrophages to form the CD200–CD200R-complex with tumor cells. Our results help understanding the complexities of tumor microenvironment.