A new study could help reveal why some vaccines, such as those for COVID-19 and influenza, are less effective in older people than in younger people, potentially fundamentally changing our understanding of aging.
Scientists have traditionally assumed that the decreased vaccine response seen in older adults is due to age-related weakening of the immune system. Many have pointed to sustained, low-grade immune activation (a process called “inflammation”) as one factor in this decline.
However, a new study comparing the immune systems of older and younger people did not find that biological markers of inflammation consistently increased with age. Instead, aging appears to reprogram T cells. T cells are important immune cells that help train a type of white blood cell called a B cell to produce antibodies in response to viruses and vaccines.
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The findings, published October 29 in the journal Nature, suggest that inflammation may not be as fundamental to the aging process as scientists previously thought.
“We believe that inflammation is driven by something independent of a person’s age alone,” Claire Gustafson, a research assistant at the Allen Institute for Immunology and one of the study’s lead authors, said in a statement.
Alan Cohen, an associate professor of environmental health sciences at Columbia University who studies aging and inflammation, said the new findings support a more nuanced view of inflammation.
Cohen, who was not involved in the study, said the idea that inflammation increases with age “may be true on average in industrialized populations.” “But that doesn’t apply to everyone, and it doesn’t apply to all populations,” he told Live Science.
Cohen cautioned that the participants in the new study were all from highly industrialized areas: Palo Alto, California, and Seattle. He found significant differences in inflammation between adult populations in Italy, Singapore, Bolivia and Malaysia, and said such findings may not hold true in different settings.
“I in no way take this as, ‘Hey, we’ve conclusively shown that inflammation doesn’t change with age,'” Cohen said. “I would like to take this as an example of a population that doesn’t seem to be doing the same things that we would normally expect.”
T-cell changes are not caused by inflammation
With the goal of improving older adults’ responses to vaccines, Gustafsson and his colleagues looked at how T cells change with age.
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First, they compared young adults (ages 25 to 35) to older groups (ages 55 to 65, or what researchers call the “peak of aging”). The researchers followed 96 healthy volunteers in these age groups for two years, taking blood samples from each participant eight to 10 times and monitoring their immune systems before and after their annual flu vaccination. The researchers then expanded the study to include a second group of 234 adults, ranging in age from 40 to over 90.
To examine the immune system across these groups, the research team used single-cell RNA sequencing. This made it possible to examine a type of genetic material called RNA inside each immune cell. RNA reflects which proteins a cell is producing at a given moment. The researchers also used high-dimensional plasma proteomics, which maps proteins circulating in the blood, and spectral flow cytometry, which identifies and enumerates immune cells by their molecular “fingerprints.”
Researchers found distinct differences in memory T cells, immune cells that “remember” past infections and help the body respond faster the next time a pathogen appears.
In older adults, the number of memory T cells increases and their interactions with B cells change, leading to a shift in the way they respond to threats. Studies have found that when memory T cells are not functioning properly, B cells are less effective at producing antibodies in response to infections and vaccines. Young adult memory T cells, on the other hand, responded quickly and were better at raising the expected antibody response.
These immune changes appear to occur independently of inflammation and latent viral infection. Latent viruses can remain in the body after the initial infection and become dormant without causing any obvious symptoms. Infections with these viruses, such as cytomegalovirus (CMV), are often cited as a cause of age-related decline in the immune system. However, the study found that people under the age of 65 who had a CMV infection at some point in their lives showed no signs of accelerated immunosenescence or increased levels of inflammatory proteins.
Professor Cohen remains cautious about the study authors’ conclusions, noting that the most significant changes in the immune system tend to occur after age 65. “If we don’t see changes in inflammation between ages 25 and 35 and between ages 55 and 65, is it really because inflammation doesn’t change with age, or are we just not old enough to know anything?” he asked.
The researchers said these findings could ultimately help scientists design vaccines that compensate for age-related immune changes and better protect older people. They also think the results could help design treatments to restore immune function in older people.
This article is for informational purposes only and does not provide medical advice.
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