Scientists at Cedars-Sinai may have discovered why some treatments for rheumatoid arthritis (RA) stop working over time.
Their research, published in the journal Science Immunology, explains how immune cells inside the joints change as the disease gets worse.
These changes may help explain why certain medications, especially those that block a protein called interleukin-17 (IL-17), don’t work well for many people with RA.
Rheumatoid arthritis is a long-term disease where the immune system attacks the joints, causing swelling, pain, and damage. About 1.5 million people in the United States are affected by this condition.
Doctors sometimes treat autoimmune arthritis by blocking IL-17, a protein that causes inflammation. But for people with rheumatoid arthritis, this treatment often doesn’t work well.
Dr. Nunzio Bottini, a lead researcher at Cedars-Sinai, explained that the joint tissue environment plays a big role in how RA gets worse and why it becomes harder to treat.
In studies using both human joint tissue and mice, the scientists found that immune cells that normally produce IL-17 slowly stop making it as the disease goes on. This means that medications targeting IL-17 have fewer targets, making them less effective.
What’s more, the immune cells don’t just become less active—they actually change in other ways. Over time, they become more aggressive and can keep causing inflammation even without IL-17. This change may be one reason why RA becomes harder to control in the later stages.
The researchers also discovered that another type of cell, called synoviocytes, plays a key role in driving these changes. Synoviocytes are not immune cells—they are found in the joints and help produce the fluid that keeps joints moving smoothly. However, in RA, they can send signals that push immune cells to become more harmful.
A special team at Cedars-Sinai that focuses on computational biology helped make this discovery by using advanced tools to study how cells behave in their natural environment. This field, called spatial biology, helps scientists understand how diseases develop inside specific tissues.
Dr. Joyce So, another expert at Cedars-Sinai, said this discovery could change how scientists and doctors think about rheumatoid arthritis. It shows that understanding the tiny details of how the disease works inside the joints is key to finding better treatments.
She also said that people in the early stages of RA may benefit more from existing treatments, and that doctors should try to treat the disease early, before these harmful changes occur.
This research offers hope that more targeted, effective treatments could be developed in the future. By knowing exactly how and why the immune system changes in RA, scientists may be able to stop the disease earlier and more successfully.
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