Objective: To assess the effects of TNF-antagonist therapy on BLyS expression in RA patients.
Methods: Blood from 38 RA patients from a single center was collected prior to and following initiation of TNF-antagonist therapy. Plasma BLyS protein levels, blood leukocyte BLyS mRNA levels, and disease activity were longitudinally monitored. Five normal healthy volunteers and 12 RA patients who either refused or were felt not be candidates for TNF-antagonist therapy served as TNF-antagonist-naïve controls.
Results: Baseline plasma BLyS protein levels, but not blood leukocyte BLyS mRNA levels, were elevated in RA patients. Plasma BLyS protein levels declined following initiation of TNF-antagonist therapy in good responders (GR) to TNF-antagonist therapy but not in poor responders (PR). In contrast, the ESR declined in response to TNF-antagonist therapy in both GR and PR. TNF-antagonist therapy did not promote change in blood leukocyte BLyS mRNA levels in either GR or PR, suggesting that the TNF-antagonist-associated changes in circulating BLyS protein levels reflected changes in local BLyS production in the affected joints rather than changes in systemic BLyS production. BLyS expression did not change over time in either the normal or RA control groups.
Conclusions: A good clinical response to TNF-antagonist therapy in RA patients is associated with a decline in plasma BLyS protein levels. Increased BLyS expression in affected joints may contribute to ongoing disease activity, and reduction of such expression may help promote a favorable clinical response to TNF-antagonist therapy.
- B lymphocyte stimulator
- rheumatoid arthritis
- tumor necrosis factor