American scientists have uncovered the primary mechanism of aging. It turns out that as we age, macrophages—immune system cells responsible for clearing cellular “waste” from the body—lose a significant portion of their functionality. They can no longer effectively eliminate spent neutrophils, and the accumulation of the latter triggers chronic inflammation, which remains one of the main drivers of aging. The findings have been published in the journal Science.
Researchers focused on studying the interaction between macrophages and neutrophils, which respond acutely to infections and inflammation. In youth, macrophages manage to swiftly engulf spent neutrophils. But with advancing age, this process becomes more difficult.
Experiments demonstrated that old neutrophils produce an excess of the protein CD47, which acts as a kind of label: “don’t eat me.” As a result, macrophages cease their timely elimination, and these neutrophils continue to sustain inflammation linked to tissue aging.
When specialists blocked the action of CD47 in elderly rodents, macrophages regained their ability to actively remove old neutrophils. This reduced inflammation levels and improved the function of certain tissues.
It is still too early to talk about creating an “anti-aging drug,” the authors of the study acknowledge. However, the results have highlighted a promising therapeutic target: by restoring immune system function, it may be possible to slow down age-related changes and lower the risks of several pathologies.
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