Mechanism discovered that leads to inflammation in rheumatoid arthritis could pave the way for new treatments

Synovial CD4+ T cells that produce IL-21 contribute to joint inflammation by activating synovial fibroblasts in people with rheumatoid arthritis, highlights new research.

Scientists isolated T cells from synovial fluid from people with rheumatoid arthritis that produced IL-21 and TNF and compared these with cells that did not produce this cytokine. When cells that produced IL-21 were put in culture with synovial fibroblasts (the main contributors to joint inflammation in rheumatoid arthritis), they induced the production of proinflammatory cytokines by these synovial fibroblasts, and cells that do not produce IL-21, did not demonstrate this same outcome.

So a combined therapy that targets IL-21 and TNF might be beneficial for people who do not respond to anti-TNF therapy or other current therapies.

“Patients with rheumatoid arthritis often become refractory to treatment provoking the need to try different drugs targeting different pathways,” explains Dr John Wherry, deputy editor of the Journal of Leukocyte Biology where the research is published. “The identification of a new inflammatory target in rheumatoid arthritis holds promise for better treatment for these patients and perhaps those with other autoimmune or inflammatory diseases.”

For more in-depth features, interviews and information, subscribe to Arthritis Digest magazine, a popular title that’s published six times a year. Click here for the digital version or tel 0845 643 8470 to order your had copy. You’ll know what your doctor is talking about, what new drugs are in the pipeline and be up to date on helpful products.