Researchers led by Cedars-Sinai Health Sciences University have discovered a protein that may allow harmful aging cells to escape detection by the immune system. By helping these cells remain in the body instead of being cleared away, the protein could contribute to their accumulation and the development of health problems associated with aging. The discovery, published in Cell Metabolism, identifies PD-L2 as a potential target for therapies aimed at eliminating harmful aging cells.
Scientists also believe the protein could serve as a blood marker, providing a way to detect and monitor these cells. "Our findings suggest that PD-L2 may help aging cells stay in the body when they would normally be removed by the immune system," said Selim Chaib, PhD, research assistant professor of Medicine at Cedars-Sinai and first and co-corresponding author of the study. How Harmful Aging Cells Escape the Immune System As cells age or become damaged, some enter a state known as senescence.
These cells stop dividing but remain alive, lingering in tissues rather than disappearing. Over time, they can accumulate and release substances that trigger inflammation and disrupt the normal activity of surrounding cells. The buildup of these senescent cells has been associated with a range of health problems that become more common with age.
Understanding why they persist, particularly when the immune system would normally remove them, could help scientists develop new ways to reduce their harmful effects. The researchers found that PD-L2 may play an important role in this process by helping aging cells avoid immune clearance. Blocking PD-L2 Reduces Aging Cells in Mice To investigate the protein's role, scientists conducted experiments in laboratory mice in which PD-L2 was either removed or blocked.
Both approaches reduced the accumulation of senescent cells and lowered levels of the inflammatory substances they release. The benefits extended beyond changes at the cellular level. Mice with reduced PD-L2 activity also showed improvements in their ability to process sugar and demonstrated greater grip strength, suggesting that targeting the protein could influence physical functions affected by aging.
The team also examined human cells and tissues. They discovered that senescent human cells produced more PD-L2 than younger cells and that levels of the protein rose with age in certain human tissues. These findings suggest the mechanism observed in mice may also be relevant to human aging.
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