Scientists have long wondered whether the immune system ages as a result of rheumatoid arthritis (RA) or whether this aging might actually help cause the disease.
A new study from the University of Birmingham now suggests the latter may be true—immune system aging could be a driver of RA, not just a consequence.
The study, published in eBioMedicine, found that signs of premature immune aging appear even before people are diagnosed with rheumatoid arthritis.
This discovery opens the door to earlier detection and possibly prevention for those at risk.
Rheumatoid arthritis is an autoimmune disease in which the immune system mistakenly attacks the body’s own joints, leading to pain, swelling, and long-term damage.
The new research involved 224 participants at various stages of the disease, from early joint pain to confirmed RA. It is one of the most detailed investigations of immune aging in rheumatoid arthritis to date.
Dr. Niharika Duggal, the study’s senior author and an associate professor of immune aging at the University of Birmingham, explained that people showing early joint symptoms already had immune systems that looked older than expected.
“We’ve discovered that immune aging isn’t just a consequence of rheumatoid arthritis—it may be a driver of the disease itself,” she said.
“These findings suggest we might be able to intercept the disease in at-risk individuals by using treatments that slow aging.”
The researchers observed that participants with early immune aging were more likely to go on to develop full-blown rheumatoid arthritis.
Their immune systems showed reduced numbers of “naïve” T cells—the young, flexible immune cells that fight new infections—and lower activity from the thymus, the organ that produces these cells. They also had higher levels of inflammatory molecules, such as IL-6, TNFα, and CRP, even before diagnosis.
Once rheumatoid arthritis became established, the immune system showed more advanced signs of aging, including the buildup of worn-out, “senescent” T cells and inflammatory Th17 cells.
The findings point to a possible new way to prevent or delay the disease by targeting the aging process itself. The researchers suggest that drugs that promote cell cleanup and repair—such as spermidine, metformin, or senolytics—might help slow immune aging and reduce the risk of developing rheumatoid arthritis.
If confirmed in future studies, this could mark a major step toward preventing autoimmune diseases before they take hold.
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