Your Immune System Ages in Two Big Bursts

Obviously our bodies change a lot as we age, and culturally we tend to focus on the ones we can see—wrinkles, weight gain, loss of muscle mass, etc. But the most dramatic alterations may be happening beneath the surface. The immune system, for example, undergoes quite a bit of remodeling as we get older. What’s going beneath the surface of that system, though?

To find out, a team of researchers led by immunologists from Duke University drilled down to the cellular level. They investigated the genetic activity of 3.8 million immune cells from close to 2,000 healthy people between the ages of 19 and 97 in Singapore, and recently published their findings in Nature Communications.

Read more: “Watch Immune System Cells Gobble Up Cancer Cells”

The team found that rather than aging gradually, these cells experience two bursts of aging around our 40s and 60s. T-cells in particular showed marked changes in their transcription and translation around these periods. Helper T-cells (which coordinate the adaptive immune response) showed altered gene expression profiles around age 40, while killer T-cells (which target and eliminate infected cells) showed altered gene expression around age 60.

And there were some important differences between the sexes. In women, killer T-cells showed a steady rise in gene activity associated with immune activation and killing infected cells. Males, on the other hand, showed an early rise that plateaued later in life. According to the team, this could help explain why older women are better at clearing pathogens and responding to vaccines, compared to older men. Unfortunately, this relatively higher immune activation in women could also contribute to inflammation.

Strikingly, in both sexes, immune cells seemed to slow down a bit with age, winding down the cellular machinery responsible for making proteins. The production of ribosome and translation initiation factors, as well as RNA processing, decline with age in immune cells, the researchers found. “The biological consequences of this decline are likely to be profound,” they wrote. “Reduced protein synthesis capacity impairs cellular stress responses, limits proliferative potential, and may promote accumulation of misfolded proteins.”

So what can we do with this information?

According to the team, it could help lead to more personalized treatments. “Understanding what drives these windows of immune aging could eventually help us identify when, and for whom, interventions may have the greatest benefit,” study author Jacques Behmoaras of Duke University explained in a statement. “It could also shed light on why some autoimmune conditions disproportionately affect women.”