Immune cells worsen sun damage in aging skin

When skin is exposed to UV radiation, the immune system responds as if an invader is present. This triggers sterile inflammation (inflammation that occurs without infection, purely in response to tissue damage). In aging skin, this response differs from how it unfolds in younger skin. The researchers published their findings in the journal Aging Cell.

The key players are neutrophils: white blood cells that arrive first at sites of damage. When activated, neutrophils can release structures called NETs (neutrophil extracellular traps), networks of genetic material and proteins designed to capture pathogens. In UV-damaged skin, NETs activate even though there is no pathogen present. The resulting structures can then damage healthy surrounding tissue instead.

Inflammaging in the skin

This mechanism fits into the broader pattern of inflammaging: the chronic, low-grade inflammation that increases with age and causes damage across many tissues. In the skin, inflammaging heightens vulnerability to UV damage. That makes aging skin more susceptible, even at the same level of sun exposure as younger skin.

In a mouse model, the researchers tested whether blocking NET formation would reduce the damage. It did. Mice in which NET activation was inhibited showed less tissue damage after UV exposure. These are preliminary findings in animal models, and the step from mouse to human remains substantial.

What this means for skin aging

For longevity science, this is relevant on multiple levels. It shows that aging changes not only cells but also how the immune system responds to damage. It also raises the possibility that targeting immune activation could be a strategy to slow skin aging. The researchers are careful to note that the findings remain at an early stage, and clinical application is not yet in sight.

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