Targeting NKG2D Ligands on the Surface of Persistent Senescent Cells Enables their Destruction by the Immune System

In conclusion, our data show how oncogenic and tumor-suppressive drivers of cellular senescence regulate surveillance processes that can be circumvented to enable SnCs to elude immune recognition but can be reversed by cell surface-targeted interventions to purge the SnCs that persist in vitro and in patients. Since eliminating SnCs can prevent tumor progression, delay the onset of degenerative diseases, and restore fitness; since NKG2D-Ls are not widely expressed in healthy human tissues and NKG2D-L shedding is an evasion mechanism also employed by tumor cells; and since increasing numbers of B cells express NKG2D ligands in NKG2D receptor-deficient mice as they age, we propose that therapeutic interventions designed to increase cell surface presentation of NKG2D-Ls could be effective senolytic strategies to resensitize persistent SnCs to immune detection and rescue their clearance, whether in cancer or aging settings.
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs