New research from Cedars-Sinai may explain why some common treatments for rheumatoid arthritis don’t work as well over time.
The findings, published in the journal Science Immunology, suggest that changes inside the joints themselves may be to blame.
Rheumatoid arthritis is a chronic autoimmune disease. This means the body’s immune system, which normally fights off germs, mistakenly attacks the joints. This causes swelling, pain, and damage over time. Around 1.5 million Americans live with this painful condition.
Doctors often treat autoimmune arthritis by blocking a protein called interleukin-17 (IL-17), which plays a role in joint inflammation. These treatments work well for some forms of arthritis. But they haven’t worked as well for people with long-term rheumatoid arthritis. Scientists wanted to understand why.
Led by Dr. Nunzio Bottini at Cedars-Sinai’s Kao Autoimmunity Institute, researchers looked at tissue samples from people with rheumatoid arthritis, as well as lab mice. They discovered that immune cells in the joints change over time.
At first, they produce IL-17, but as the disease progresses, they stop making it. That could explain why drugs that block IL-17 stop working—they’re no longer targeting the right part of the disease process.
But the problem is more complex. The immune cells don’t just stop making IL-17. They also become more aggressive. Even without IL-17, these cells can continue to drive inflammation and damage in the joints. That’s one reason the disease can continue to get worse, even when treated.
The study also found that these changes in immune cells are triggered by other cells in the joint, called synoviocytes. These are not immune cells—they normally make the fluid that helps joints move smoothly. But in rheumatoid arthritis, they seem to change the behavior of immune cells, making the disease harder to treat.
To understand this process, the researchers used a new tool called spatial biology, which allows scientists to study how cells behave within the actual tissue environment. The Department of Computational Biomedicine at Cedars-Sinai helped lead this part of the study.
Dr. Joyce So, a genomics expert at Cedars-Sinai, said the findings are important because they help explain why some treatments fail. If doctors can better understand how and when these changes happen, they might be able to create more effective treatments.
One important takeaway from this research is the need for early treatment. In the early stages of rheumatoid arthritis, IL-17 blockers might still work. But as the disease progresses and the immune cells change, those drugs become less effective. That’s why doctors and patients need to act quickly when symptoms begin.
This study shows that rheumatoid arthritis is not a simple disease. It changes over time, and the way it should be treated might need to change as well. Researchers hope that by understanding the timing and nature of these changes, they can develop “precision therapies” that are better matched to each patient’s stage of disease.
More research is needed, but this discovery offers hope. By learning how the immune system and joint cells interact, scientists may be able to stop the disease earlier and more effectively.
If you care about pain, please read studies about how to manage gout with a low-purine diet, and a guide to eating right for arthritis.
For more health information, please see recent studies about the link between processed foods and chronic diseases, and avoid these 8 foods to ease arthritis pain.
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