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Background Radiation therapy (RT) can stimulate antitumor immunity via cGAS-STING-mediated dendritic cell activation. However, RT also suppresses the immune response to tumors through lymphodepletion, reduced lymphocyte reactivity, and unfavorable shifts in T cell subpopulations. Understanding how these competing effects interact is critical for optimizing RT-immunotherapy combinations, particularly with respect to RT dosing and timing of immunotherapy relative to RT administration.Methods We are developing a computational model to simulate the net immune consequences of RT. The model includes terms to account for RT-dose-dependent initiation of immune-mediated cell death, as well as factors contributing to RT-induced immunosuppression, including baseline absolute lymphocyte count (ALC), rate of ALC loss during RT (dependent on RT dose per fraction, number of fractions, target volume size, and body site treated), and timing of RT relative to immune checkpoint blockade.Results The model explores scenarios in which immunostimulatory effects of RT may outweigh immunosuppressive effects, and vice versa, across a range of treatment conditions. Planned simulations will identify thresholds and parameter regimes associated with net immune activation or suppression.Conclusions This framework will generate testable hypotheses about how RT modulates antitumor immunity and inform rational design of combination therapies. Future model extensions will incorporate lymphocyte subpopulation dynamics, tumor radiosensitivity, and site-specific effects to improve biological fidelity and clinical relevance.