Synovial inflammation associated with rheumatoid arthritis (RA) is exacerbated by over-expression of lymphotoxin (LT)-β-related genes, scientists report in the journal Rheumatology International.
Biological therapies are associated with dramatic results in certain individuals with RA. However, such therapies fail completely in other patients, highlighting the need for a better understanding of the pathogenesis of this disease.
For their study, Killian O'Rourke (Musgrove Park Hospital, Taunton, UK) and co-workers investigated the expression of LT-β-related genes, which produce a protein that has been implicated in lymphoid follicle development and the production of pro-inflammatory cytokines, fibroblasts, and synoviocytes.
The 21 RA patients studied were found to have significantly higher levels of synovial LT-β expression than 20 generally healthy control volunteers who were undergoing arthroscopy for non-inflammatory joint conditions.
Furthermore, higher levels of LT-β gene expression were shown to correlate significantly with greater synovial inflammation and higher pain scores in RA patients.
The researchers point out that anti-LT-β proteins have already been successfully used to reverse the inflammation associated with diabetes, colitis, and graft-versus-host disease in animal models.
The authors believe that their findings "could be exploited to facilitate a rationale for the treatment of selected RA patients, with a therapy to modulate LT-β pathways, which could potentially ameliorate RA inflammatory pathways."