Two people born on the same day can end up with very different immune systems in old age: some stay resilient, others become worn down in ways that raise the risk of age-related disease1. A study published on October 9 in the journal Immunity tries to explain why, using what its authors call a map of human immune aging1. The team, from Washington University School of Medicine in St. Louis (WashU), Nationwide Children’s Hospital in Ohio and King’s College London, reports that the balance between two kinds of white blood cells tracked who later got sick or died2.
This is the first Biohack article on this subject. It is a finding about patterns in blood, not a new treatment.
What the researchers did
The team analyzed about 12.4 million individual immune cells from the blood of 2,609 mainly healthy adults, drawn from eight groups of volunteers in North America, the UK, Asia and Australia1. They sorted the cells into 59 distinct types, a fine level of detail that let them separate closely related T cells (a kind of white blood cell) that older methods cannot reliably tell apart3. King’s College London’s team supplied 188 of the blood samples, from younger and older adults in its own aging research2.
Younger people’s blood looked much the same from person to person. It was rich in “naive” immune cells, ones that have not yet met a specific germ and can still adapt to new infections or vaccines1. Older people’s blood varied far more, and some older participants carried more cells that reflect inflammation1. In Eric Topol’s summary of the paper, the loss of naive T cells was the strongest predictor of a person’s actual age in the study4.
A tale of two cell types
The researchers focused on effector memory CD8 T cells, immune cells that “remember” past germs. These cells carry granzymes, which WashU describes as molecular weapons used to destroy target cells or coordinate immune responses1. Some make mostly granzyme B and act as direct destroyers of diseased cells. Others make granzyme K; these are less studied and may help call in immune backup1.
Each person was placed on a spectrum based on the ratio between these two cell types1. According to the universities, a healthy immune system gradually shifts toward granzyme K cells over time, while one leaning toward granzyme B cells signals unhealthy aging2. In Topol’s reading of the paper, cytomegalovirus (CMV, a common virus) infection and chronic diseases such as heart disease or type 2 diabetes push the immune system toward granzyme B cells4. People who carried CMV had more granzyme B cells, and people with higher levels of C-reactive protein, a blood marker of inflammation, had a larger share of them4. Live Science reported that people with a lower ratio of K to B cells were more likely to have autoimmune or other chronic immune conditions5.
Linking the cells to later illness and death
The next question was whether a healthy person’s place on the spectrum predicted future health. For this the team used the UK Biobank, which followed 500,000 initially healthy people aged 40 to 69 and recorded their medical events for up to 15 years1. The Biobank has measurements of hundreds of blood proteins but no counts of CD8 T cells1.
To work around this, the researchers used a smaller group of seemingly healthy adults who had both cell counts and blood protein data. From it they built a computer model of the protein “tracks” left when granzyme B or granzyme K cells dominate1. Live Science reported that this step used 329 people5. The model was then applied to stored blood protein samples from about 50,000 Biobank participants1.
Healthy adults whose immune systems leaned heavily toward granzyme B cells at the start had a higher risk of death a decade later than those with more granzyme K cells1. The granzyme B group was also more likely to develop chronic conditions over the following decade, including type 2 diabetes, high blood pressure, liver disease and kidney failure1. Topol noted that the measure did not predict Alzheimer’s disease, Parkinson’s disease, dementia or age-related macular degeneration, an eye disease4.
The sources give slightly different figures. WashU says about 50,000 Biobank participants and up to 15 years of records1. Topol cites 48,620 participants with 17 years of follow-up4, and Live Science says around 48,0005. Age ranges also differ: 20 to 90-plus in the university releases1, 18 to 98 in Topol’s summary4.
“A higher level of granzyme B cells in a healthy state means the immune system might be already reacting to something. It isn’t a formal disease diagnosis, but it may indicate the body is off track.”
That was co-author Marina Terekhova of WashU Medicine1.
What it does not show yet
Topol, who called the paper one of the most important in the science of aging, also listed its limits4:
- Participants were mainly of European and Asian ancestry, so it is unclear whether the results apply to people of African ancestry4.
- Only blood was studied, not tissues4.
- The cell balance was measured once, so it is not known how it changes within a person or whether lowering it changes risk4.
- Calling K cells “good” and B cells “bad” is an oversimplification, since K cell granules can also promote inflammation4.
- T cell counts in the Biobank were estimated with a model, not measured4.
- None of the work establishes cause and effect4.
The same team’s earlier research found that granzyme K cells built up in several tissues of old lab mice and were linked to inflammation, Live Science reported5. That was an animal finding, and it shows the picture of which cell type is harmful is still being worked out.
King’s College London’s Stephen Harridge said in the university’s release that physical activity, a balanced diet and a healthy body weight help reduce inflammation and keep the immune system healthy2. That is his view; the sources do not describe the study testing any lifestyle change.
Who is behind it
The study was led by Maxim N. Artyomov, a professor of pathology and immunology at WashU Medicine, with co-corresponding authors Stephen Harridge of King’s College London and Mykyta Artomov of Nationwide Children’s Hospital2. The sources reviewed do not describe who funded the work. The researchers have made the combined dataset publicly available3.
Artyomov’s lab is adapting the research into a simple blood test that could run on standard equipment, since placing someone on the spectrum today requires complex and costly technology1. “We can think of it like checking a car’s oil level before the check engine light ever turns on,” Artyomov said1. No such test exists yet in these sources.
How it fits the field
Other groups are building similar immune maps. A separate study from Duke-NUS Medical School in Singapore, published in Nature Communications, analyzed 3.8 million immune cells from nearly 2,000 healthy people aged 19 to 976. It found that blood immune cells do not age at a steady pace, with major shifts in gene activity around age 40 and again after 60, driven mainly by T cells and differing between men and women6. That work was funded by Singapore’s National Research Foundation and other government bodies6. It is a different study from the WashU-led one, and the two did not measure the same thing.
The Allen Institute for Immunology has also published, in Nature in 2025, a study that followed 49 younger and 47 older healthy adults for two to three years, profiling over 13.5 million blood cells7. Unlike the single snapshot in the WashU-led study, that project sampled the same people repeatedly7.
What to watch next
- Whether the WashU team produces a simpler, cheaper blood test and checks it in new groups of people1.
- Studies that measure the cell balance repeatedly in the same people, which Topol flagged as missing4.
- Results in more diverse populations, including people of African ancestry4.
- Any trial testing whether shifting the balance changes disease risk; none is described in these sources.
