Cytokine-induced ‘bystander ’ senescence in DDR and immuno- surveillance

Cells with damaged and unrepaired genomes represent a potential threat for the organism and therefore their elimination is beneficial. The biological safeguard barriers responsible for elimination of such hazardous cells rely on two principles: intrinsic- achieved through cellular senescence/apoptosis, and extrinsic- performed by the immune system. The concept of immune system-mediated clearance of senescent cells is well established [1], however the exact mechanisms and modes of mutual interplay between cellular senescence and immune surveillance are only emerging. Research performed in the last two decades shows that cellular senescence as an essentially irreversible block of cell proliferation can be triggered or bypassed via manipulation of expression levels of several dozens of genes indicating the complexity and redundancy of regulatory machinerie