In addition to direct cell death via DNA damage, RT may promote tumor-specific immune responses through:
Release of tumor antigens and other molecules collectively known as damage-associated molecular patterns (DAMPs). In particular, DNA particles in a cell's cytosol can trigger the cGAS-STING pathway which triggers the transcription of inflammatory genes and ultimately activates an innate immune response. (STING = STimulator of Interferon Genes)
Increased tumor-specific antigen expression
Upregulation of MHC antigen presentation
Decreased expression of immunosuppressive ligands, like PD-L1
Upregulation of proteins that support T-cell adhesion, tethering and chemotaxis in tumor-micro-environment