Novel Mechanism Induces Joint Destruction in Rheumatoid Arthritis


Synovial CD4+ T cells that produce IL-21 play a role in joint inflammation.

A mechanism that plays a role in joint inflammation in patients with rheumatoid arthritis (RA) has been identified, which could present a new treatment target.

Destruction to bone and cartilage is one of the key manifestations of RA. Scientists have known the role of T helper (Th)17 cells in these processes, but the role of IL-21-producing T cells has not been as clear.

In a study published in the Journal of Leukocyte Biology, sought to examine the role of IL-21 in RA by focusing on the functional characteristics of synovial IL-21/TNF-producing CD4 T cells.

The investigators used a novel method to isolate T cells from synovial fluid from patients with RA that produced IL-21 and TNF. These were then compared with cells that did not produce the cytokine.

When cells that produced IL-21 were put in culture with synovial fibroblasts, the results of the study showed that they induced the production of proinflammatory cytokines by the synovial fibroblasts. Cells that did not produce IL-21 did not demonstrate the same outcome.

The findings suggest that a combination therapy that targets IL-21 and TNF may be beneficial for patients who do not respond to anti-TNF therapy or other current therapies. Furthermore, the findings could also have an impact on diseases such as systemic lupus erythematosus, systemic sclerosis, and Crohn’s disease.

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

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