Immunology and Rheumatoid Arthritis

What causes rheumatoid arthritis?

In RA, immune cells target the synovium, the thin layer of tissue that lines the joints. Researchers aren’t exactly sure what causes the immune system to make this mistake, but genetics and environment play a role.

How does the immune system cause rheumatoid arthritis?

As with other autoimmune disorders, RA occurs when the immune system mistakenly makes autoantibodies, which are antibody proteins that mark parts of the body for attack instead of targeting harmful pathogens. Immune cells called T cells coordinate this misdirected attack, and B cells produce the autoantibodies. Immune cells also release inflammatory signals called cytokines, which drive inflammation associated with RA. As the synovium becomes inflamed and crowded with immune cells, it thickens, which causes some of the joint stiffness associated with RA.

What are Researchers Uncovering About Rheumatoid Arthritis?

Immunology research can help uncover how the disease begins and progresses over time. This knowledge could lead to improved diagnosis or treatments that address the autoimmunity of rheumatoid arthritis rather than just the symptoms.

When do changes in the immune system that lead to RA begin?

Researchers at Allen Institute recently mapped how the immune system changes in individuals at an increased risk of developing RA. They found that people at risk for RA had significant changes in their immune system long before they felt the symptoms. This meant the immune system was building autoimmunity long before they had any idea. This research can help researchers develop earlier treatments and diagnoses for RA, maybe even saving patients years of pain.

Why do some people with RA not respond well to standard treatments?

Researchers at Mass General Brigham Hospital in Boston, MA, wanted to understand why some people with RA do not respond well to standard treatments. The researchers looked at tissues from the joints of patients before and after they received treatment to see if they could identify anything that affected treatment success. They found that the joints of patients who did not respond well to treatment tended to have extra scar tissue, or fibrogenesis. This prevented the treatments from reducing joint pain, even if it reduced the immune response. Understanding why some patients don’t respond well to treatment could help researchers develop different treatment options for these patients.