Similar to immune reactions against antigens from bacteria or viruses, the<unk>  requires priming of immune cells against tumor antigens. Local irradiation of a tumor nodule may lead to immunogenic forms of tumor cell death and liberation of tumor cell-derived antigens. These antigens can be recognized and processed by antigen-presenting cells within the tumor (dendritic cells and macrophages). Cytotoxic T cells which recognize these tumor antigens may in turn be primed by the tumor antigen-presenting cells. In contrast to the local<unk>  of irradiation on the tumor cells, these cytotoxic T cells circulate through the blood stream and are thus able to destroy remaining tumor cells in distant parts of the body which were not irradiated. Accordingly, increases in tumor-specific cytotoxic T cells were shown to correlate with<unk>  anti-tumor responses in patients. Vice versa, the<unk>  is abolished after experimental depletion of T cells in various animal models.<unk> s of ionizing radiation are often blocked by the immunosuppressive microenvironment inside the irradiated tumor which prevents<unk> ive T cell priming. This explains why the<unk>  is so rarely seen in patients receiving radiotherapy alone. In contrast, the combination of immunomodulatory drugs such as ipilimumab and pembrolizumab can partially reconstitute systemic anti-tumor immune reactions induced after local tumor radiotherapy. The optimal combination of radiation dose and fractionation with immunomodulatory drugs is currently under intensive investigation. In this context, it was proposed that radiation doses above 10 to 12 Gray might be ineffective in inducing immunogenic forms of cell death. However, there is so far no consensus on the optimal radiation regimen needed to increase the chance of<unk>  tumor regression.
Abscopal effect
Rebound effect
Windkessel effect
Central tolerance
Neutral stimulus
Tetanic contraction
Gateway drug effect
Haldane effect