At baseline, both the tumor immune microenvironment and the poor antigenicity of the tumor
allow it to escape immune recognition. Targeted RT can induce increased antigenic expression,
release pro-inflammatory cytokines (e.g., CXCL16) that recruit immune cells, promote antigen
cross-presentation (HMGB-1 via TLR4), and induce tumor expression of death receptors.
Anti-CTLA4–targeted immunotherapy can enhance the adaptive immune component by
promoting antigen cross-presentation and T cell activation. Used together, RT and
immunotherapy may have synergistic effects and may shift the tumor immune system balance
toward elimination.