The mechanisms of LTB4-induced migration and invasion in fibroblast-like synoviocytes (FLS)

Rheumatoid arthritis (RA) is a chronic, systemic inflammatory disease that primarily targets synovial tissues, which forms the joint lining and produces lubricating and cushioning synovial fluid. It is relatively common with a prevalence of approximately 1% in adults worldwide.

To create new therapies to fight this inflammation, the mechanisms causing inflammation must be understood. Fibroblast-like synoviocytes (FLS), the major cellular populations in the synovial lining, directly contribute to inflammatory arthritis through aggressive invasion into the cartilage and bone. Dr. Chen’s lab has demonstrated a critical role of leukotriene B4 (LTB4), an inflammatory mediator, in inflammatory arthritic mouse models. Dr. Chen’s project seeks to understand the role of LTB4 in synovial inflammation in the pathogenesis of inflammatory arthritis.

Defining these mechanisms in the mouse will permit focused exploration of similar mechanisms in humans. Ultimately, such work may eventually provide new therapeutic options for patients with rheumatoid arthritis.