Radiation-induced equilibrium is a balance between tumor cell proliferation and T cell–mediated killing
The Journal of Immunology, 2013•journals.aai.org
Local failures following radiation therapy are multifactorial, and the contributions of the tumor
and the host are complex. Current models of tumor equilibrium suggest that a balance exists
between cell birth and cell death due to insufficient angiogenesis, immune effects, or
intrinsic cellular factors. We investigated whether host immune responses contribute to
radiation-induced tumor equilibrium in animal models. We report an essential role for
immune cells and their cytokines in suppressing tumor cell regrowth in two experimental …
and the host are complex. Current models of tumor equilibrium suggest that a balance exists
between cell birth and cell death due to insufficient angiogenesis, immune effects, or
intrinsic cellular factors. We investigated whether host immune responses contribute to
radiation-induced tumor equilibrium in animal models. We report an essential role for
immune cells and their cytokines in suppressing tumor cell regrowth in two experimental …
Abstract
Local failures following radiation therapy are multifactorial, and the contributions of the tumor and the host are complex. Current models of tumor equilibrium suggest that a balance exists between cell birth and cell death due to insufficient angiogenesis, immune effects, or intrinsic cellular factors. We investigated whether host immune responses contribute to radiation-induced tumor equilibrium in animal models. We report an essential role for immune cells and their cytokines in suppressing tumor cell regrowth in two experimental animal model systems. Depletion of T cells or neutralization of IFN-γ reversed radiation-induced equilibrium, leading to tumor regrowth. We also demonstrate that PD-L1 blockade augments T cell responses, leading to rejection of tumors in radiation-induced equilibrium. We identify an active interplay between tumor cells and immune cells that occurs in radiation-induced tumor equilibrium and suggest a potential role for disruption of the PD-L1/PD-1 axis in increasing local tumor control.
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