MBI Publications

MBI Publications for Kang-Ling Liao (4)

  • K. Liao, X. Bai and A. Friedman
    The role of CD200-CD200R in tumor immune evasion
    J. Theor. Biol. (2013) (Accepted)

    Abstract

    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 €œaffinity€? of the macrophages to form the CD200-CD200R-complex with tumor cells. Our results help understanding the complexities of tumor microenvironment.
  • K. Liao, X. Bai and A. Friedman
    The role of CD200-CD200R in tumor immune evasion.
    Journal of theoretical biologyVol. 328 (2013) pp. 65-76

    Abstract

    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.
  • K. Liao and Y. Lou
    The effect of time delay in a two-patch model with random dispersal.
    Bulletin of mathematical biologyVol. 76 No. 2 (2014) pp. 335-76

    Abstract

    We consider a two-patch model for a single species with dispersal and time delay. For some explicit range of dispersal rates, we show that there exists a critical value ?c for the time delay ? such that the unique positive equilibrium of the system is locally asymptotically stable for ? ?[0,?c) and unstable for ? > ?c .
  • K. Liao, X. Bai and A. Friedman
    Mathematical modeling of interleukin-27 induction of anti-tumor T cells response.
    PloS oneVol. 9 No. 3 (2014) pp. e91844

    Abstract

    Interleukin-12 is a pro-inflammatory cytokine which promotes Th1 and cytotoxic T lymphocyte activities, such as Interferon-[Formula: see text] secretion. For this reason Interleukin-12 could be a powerful therapeutic agent for cancer treatment. However, Interleukin-12 is also excessively toxic. Interleukin-27 is an immunoregulatory cytokine from the Interleukin-12 family, but it is not as toxic as Interleukin-12. In recent years, Interleukin-27 has been considered as a potential anti-tumor agent. Recent experiments in vitro and in vivo have shown that cancer cells transfected with IL-27 activate CD8+ T cells to promote the secretion of anti-tumor cytokines Interleukin-10, although, at the same time, IL-27 inhibits the secretion of Interferon-[Formula: see text] by CD8+ T cells. In the present paper we develop a mathematical model based on these experimental results. The model involves a dynamic network which includes tumor cells, CD8+ T cells and cytokines Interleukin-27, Interleukin-10 and Interferon-[Formula: see text]. Simulations of the model show how Interleukin-27 promotes CD8+ T cells to secrete Interleukin-10 to inhibit tumor growth. On the other hand Interleukin-27 inhibits the secretion of Interferon-[Formula: see text] by CD8+ T cells which somewhat diminishes the inhibition of tumor growth. Our numerical results are in qualitative agreement with experimental data. We use the model to design protocols of IL-27 injections for the treatment of cancer and find that, for some special types of cancer, with a fixed total amount of drug, within a certain range, continuous injection has better efficacy than intermittent injections in reducing the tumor load while the treatment is ongoing, although the decrease in tumor load is only temporary.

View Publications By