UC Davis Health researchers have uncovered the role of cytokines in promoting the growth of synovial cells, contributing to the tissue buildup seen in psoriatic arthritis. The study elucidates the molecular mechanisms behind this autoimmune disease, where T-cells attack healthy joint tissue, causing inflammation and excessive cell growth. Focusing on synovial cells, which line joints and produce lubricating fluid, the research highlighted how cytokines drive the proliferation of these cells and contribute to pannus formation—a thick layer of inflamed tissue that damages joints and causes significant pain and mobility loss in patients. The research specifically looked at the JAK/STAT enzyme pathway in T-cells, which typically regulates genes related to immune response but can contribute to autoimmune disorders when malfunctioning. In the case of psoriatic arthritis, the activation of this pathway by inflammatory cytokines results in rampant growth of synovial cells. The study’s findings suggest that inhibiting the JAK enzyme can reduce this abnormal growth, pointing to JAK inhibitors as a promising treatment for mitigating joint damage and improving patient outcomes.

Reference: Baxt J. New research explains mechanisms behind psoriatic arthritis. UC Davis Health. Updated January 24, 2024. Accessed May 2, 2024. https://health.ucdavis.edu/news/headlines/new-research-explains-mechanisms-behind-psoriatic-arthritis/2024/01