fig2

Figure 2. Stage-dependent crosstalk between cellular senescence and tumor immunity. During the acute or early stage, STCs may exhibit increased immunogenicity and release immunostimulatory mediators that promote dendritic-cell maturation and the recruitment of NK cells and CD8⁺ T cells. Senescence-associated endothelial activation and vascular remodeling may additionally facilitate lymphocyte adhesion, transendothelial migration, and intratumoral infiltration. By contrast, persistent or chronic senescence establishes an immunosuppressive niche through immune-checkpoint upregulation, recruitment of suppressive immune populations, profibrotic and immunosuppressive SASP signaling, myeloid-cell reprogramming, and vascular dysfunction. Concurrently, senescent CD8⁺ T cells exhibit impaired proliferation and cytotoxicity, collectively promoting immune resistance, tumor progression, and metastatic dissemination.