New research from Stanford Medicine, conducted in mice and human cells, identifies a specific immune system failure that may contribute to the aging process. The study found that tissue-resident macrophages, immune cells that permanently reside within organs, become less effective with age at disposing of senescent neutrophils, another class of immune cells. This decline in macrophage function appears to contribute to aging throughout the body.
The researchers discovered that blocking a single receptor (EP2) on these macrophages, which normally responds to a hormone involved in inflammation and pain, led to multiple organs in mice retaining more youthful characteristics. The effects were observed in the brain, heart, skeletal and heart muscle, liver, spleen, bone marrow, kidney, and colon. Disabling the EP2 receptor specifically in tissue-resident macrophages also protected mice from several age-related problems, including frailty, excess fat accumulation, heart issues, and cognitive decline. The findings suggest a potential drug strategy that could slow age-related deterioration in organs and extend healthy years. [Source: https://www.sciencedaily.com/releases/2026/09/260901011717.htm]