August 18, 2025, 12:02 pm | Read time: 4 minutes
Immune defenses that function in old age as they do in youth are considered desirable. However, a recent study shows that a youthful immune system in older age can also cause harm.
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As part of the natural aging process, the human immune system weakens over the years.1 One reason for increased susceptibility to infections in old age is that fewer new T-cells are produced, as the thymus—the maturation organ for T-cells—shrinks. T-cells recognize and destroy harmful cells in the body and activate other parts of the immune system. Because the immune system weakens with age, people with an active immune system seem to have an advantage. But: This supposed youthful immunity can apparently also be harmful.
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Details of the Study
A research team from the U.S.-based Mayo Clinic found, after evaluating health records of around 22 million people, that many autoimmune diseases only appear in older age. At the same time, it is known that general immune defense weakens with age.2 From this paradox, the researchers concluded that the immune system in older age is not just still active but sometimes possibly too active. In autoimmune diseases, a malfunction of the immune system is known to occur, leading the body to attack its own tissue.
Researchers Found Immune Cells in Diseased Tissue of Giant Cell Arteritis Patients
Next, the scientists examined aortic sections from more than 100 patients over 50 years old, who are being treated for giant cell arteritis at the U.S.-based Mayo Clinic. This is a rarer, inflammatory autoimmune disease of the large and medium arteries, often affecting the cranial arteries and aorta. The Mayo Clinic is globally renowned for its expertise in complex diseases, including giant cell arteritis (GCA).3
The researchers found an increased presence of specialized immune cells, known as stem cell-like T-cells, in the diseased tissue of the patients. As a reminder: The previously mentioned T-cells are normally responsible for fighting infections as part of the immune system. These special T-cells behave similarly to T-cells in young organisms, as they can renew themselves and continuously produce new defense cells. However, in the presence of giant cell arteritis, this seemingly beneficial effect appears to be misguided. Instead of protecting the body from invaders, these cells continuously supply new T-cells that attack the blood vessels of those affected. Their efficiency thus causes significant damage.
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How a Youthful Immune System Attacks Its Own Cells
With increasing age, more new, unusual protein forms accumulate in the body, the study authors write: so-called neoantigens. The immune system has not yet developed tolerance to these proteins. “This will inevitably lead to an increase in autoimmune diseases in old age,” it continues. Normally, the immune system prevents these neoantigens from attacking its own cells. However, with age, these control mechanisms can be disrupted—a possible explanation for why autoimmune diseases occur more frequently in old age.
The study’s results suggest that autoimmune diseases in old age are not solely a result of weaker defenses. In summary, a combination of “youthful” T-cells and an increasing number of new antigens seems to lead to the immune system being unable to stop certain inflammations in old age. Part of the immune system remains too efficient, and this can be harmful to the aging body.
Significance of the Study and Limitations
The observations could offer new perspectives for medical practice—at least if the findings are confirmed in further studies. The research team plans to develop diagnostic tests to help identify autoimmune pathology in older adults. For study author Dr. Jörg Goronzy, the results are already significant for general perception. “Contrary to popular belief, a moderate aging of the immune system can indeed be beneficial,” he says. This is because moderate aging of the immune system can prevent those neoantigens from attacking the body’s own cells. However, it should be noted that the study is based on existing research. No new experiments were conducted, but existing data were interpreted. Whether the observations can be applied to other autoimmune diseases remains open—as does the question of how the specific stem cell-like T-cells contribute to autoimmune pathology. FITBOOK has reached out to the authors with these and other questions. A response is still pending.