Breakdown of immune cells’ interaction is key driver in aging, study finds

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The decline of particularly voracious immune cells called macrophages (shown above) appears to drive our organs’ decline as we age, Stanford Medicine researchers have found.

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Aging & Geriatrics July 16, 2026

Breakdown of immune cells’ interaction is key driver in aging, study finds

By Bruce Goldman

Two immune cell types’ contact plays a major role in aging. Blocking a hormone’s influence on one of those cell types halted mice’s age-associated decline in multiple organs.

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We may age at different rates, but none of us escapes aging. A study in mice and in human cells by Stanford Medicine researchers pins much of the blame on a particular type of immune cell’s increased inability, with advancing age, to gobble up another immune cell type.<br>\nSo-called tissue-resident macrophages appear to be central coordinators of age-related organ decline. Blocking a single receptor on these cells preserved the youthfulness of multiple organs in mice including the brain, heart, skeletal and heart muscle, liver, spleen, bone marrow, kidney, and colon. The receptor binds specifically to a hormone known to cause inflammation and pain in humans as well as mice.<br>\nIn mice, selectively disabling this receptor exclusively on tissue-resident macrophages prevented chronic-inflammation-driven disorders of age including frailty, excessive fat accumulation and heart trouble; it also substantially slowed cognitive decline, said Katrin Andreasson, MD, the Edward F. and Irene Thiel Pimley Professor in Neurology and Neurological Sciences.<br>\n“We’ve been trying to figure out why we age,” Andreasson said. “Now we know at least one big reason for it.”<br>\nThe study’s findings are described in a paper published online July 16 in Science. Andreasson is the senior author, and the lead author is Jessy Tan, PhD, an instructor in neurology.<br>\nThis discovery clarifies systemic inflammation’s outsized contribution to aging and the debilities that accompany it. And it suggests a pharmaceutical approach that could restrain our organs’ ineluctable march to senescence, extending our overall health spans.<br>\nA tale of two cell types<br>\nThe most abundant white blood cells in our immune system are neutrophils, our bodies’ main first responders. Born in the bone marrow, new neutrophils hop into the bloodstream, where they circulate and, if they come across a bacterial, viral or fungal pathogen, go all medieval on it: They squirt out poison and perform a hara-kiri horror act, spilling their guts out and unloading long, stringy macromolecules that form weblike nets and trap the pathogen.<br>\nPerhaps unsurprisingly, neutrophils are extremely short-lived: They’re lucky to survive 24 hours (12 hours is more typical). Some 90% of circulating neutrophils end up in the liver, spleen and bone marrow, awaiting execution and riddance by another batch of immune cells.<br>\nThis neutrophil clearance is critical. In aged animals, the vast bulk of neutrophils that never see combat undergo a fast transition to senescence, a zombie-like state in which they injure, age and inflame neighboring cells by vomiting toxic chemicals and otherwise behaving like an addled rock star punching holes in a hotel room wall.<br>\nThe older we get, the more our neutrophil counts rise, with senescent neutrophils constituting an ever higher percentage.<br>\n“Senescent neutrophils are killing our tissues,” Andreasson said. “Clearance of these cells is essential for preventing chronic inflammation.”<br>\nThat’s a job for another type of immune cell called a macrophage. These cells are by turns soldiers, builders, medics and garbage collectors. They comb the tissues for pathogens, chew them up, spurt signaling substances that summon other cells to lend a hand, and pump out growth factors that help repair damaged tissue.<br>\nFirst and foremost, Andreasson said, “They’re the body’s garbage collection crew. A lot of that garbage is defunct cells.” And a lot of those cells are neutrophils — to the tune of 100 billion a day.<br>\nMacrophages come in several subtypes. Tissue-resident macrophages are long-lived and ubiquitous. They take up residence in each of the body’s organs during fetal development and remain for their lifetimes in whatever organ they’ve inhabited, adapting their roles to fit that organ.<br>\nOne of tissue-resident macrophages’ prime responsibilities is to swallow senescent cells. Especially important targets for this operation, the study showed, are some 100 billion neutrophils, produced daily, which start showing signs of senescence within 8 to 12 hours after entering the bloodstream. (Neutrophils that haven’t arrived at...