One Immune Receptor May Drive Aging Across the Body

New research from Stanford Medicine, conducted in mice and human cells, suggests aging may be driven largely by a single immune breakdown. As animals age, tissue-resident macrophages lose their ability to clear worn-out neutrophils, letting these cells turn senescent and fuel chronic, body-wide inflammation. Blocking a receptor called EP2 on these macrophages restored that cleanup process, leaving old mice leaner, stronger, and sharper in memory tests, with brain, heart, liver and kidney tissue staying markedly more youthful. Similar patterns of neutrophil buildup and EP2 activity turned up in aging human liver cells, though no approved drug yet exists to target EP2 selectively.