Figure 7.
Figure 7. A schematic representation of the MC38-mediatedtrans-activation of NK cells. In IL-15 Tg mice, the constitutive presence of IL-15 activates NK (and CTL) cells to enhance cytokine-induced lysis of MC38 cells, resulting in the efficient rejection of these tumor cells (top). If the MC38 cells express IL-15Rα on their surface, the endogenously produced IL-15 in mice can be captured and be presented intrans to NK/CTL cells in the neighborhood (left). This scenario explains the reduced growth or lack of growth of MC38/IL-15Rα transfectants in normal mice. Hypothetically, it is plausible that administration of dendritic cells that have been engineered or activated to express IL-15Rα may activate NK/CTLs, and thus leads to activation of immune-surveillance mechanism against tumor cell development in vivo.

A schematic representation of the MC38-mediatedtrans-activation of NK cells. In IL-15 Tg mice, the constitutive presence of IL-15 activates NK (and CTL) cells to enhance cytokine-induced lysis of MC38 cells, resulting in the efficient rejection of these tumor cells (top). If the MC38 cells express IL-15Rα on their surface, the endogenously produced IL-15 in mice can be captured and be presented intrans to NK/CTL cells in the neighborhood (left). This scenario explains the reduced growth or lack of growth of MC38/IL-15Rα transfectants in normal mice. Hypothetically, it is plausible that administration of dendritic cells that have been engineered or activated to express IL-15Rα may activate NK/CTLs, and thus leads to activation of immune-surveillance mechanism against tumor cell development in vivo.

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