These cells interact with immunosuppressive cells, such as myeloid derived suppressor cells and regulatory T cells, exacerbating the state of immune exhaustion.

Characterized by a pro-inflammatory phenotype, senescent cells secrete a range of cytokines and chemokines known as the senescence-associated secretory phenotype (SASP).

This secretion contributes to a low-grade chronic inflammatory state that supports both cellular senescence and immune senescence within tissues.

Moreover, senescent cells express ligands for inhibitory immune checkpoint receptors, which serve as 'don't eat me' signals, allowing them to evade immune surveillance.

Inhibitory checkpoint pathways, particularly involving PD-1 and PD-L1, are crucial in the immune response to these senescent cells.

Overall, the interplay between senescent cells and the immune system highlights the complex mechanisms that drive aging and immune dysfunction.

Senescent cells play a significant role in the aging process by inducing an immunosuppressive phenotype in various immune cells, which promotes immune senescence.