The immune clearance of senescent cells weakens with age, leading to their accumulation and the release of inflammatory substances that contribute to aging and age-related diseases. Understanding how the immune system fails could pave the way for new senolytic therapies to remove these cells. Research from Deciduous Therapeutics suggests that senescent cells may exploit immune checkpoints to evade clearance, similar to mechanisms seen in cancer immunology. This insight could help in developing strategies to target senescent cells effectively.
The build-up of pro-inflammatory senescent cells, known as senescence-associated secretory phenotype (SASP), is a key feature of aging and age-related diseases. There’s ongoing debate on whether this accumulation is due to increased generation or impaired elimination of senescent cells in aging tissues. Recent studies highlight elevated expression of immune checkpoint ligands, like PD-L1, in senescent cells. These ligands may inhibit immune surveillance and facilitate the persistence of senescent cells by interfering with the function of cytotoxic immune cells.
Exploring these inhibitory pathways could shed light on how senescent cells evade immune clearance in aging and diseases. Enhanced inhibitory checkpoint signaling may hinder the removal of senescent cells from tissues, promoting the aging process.
