Objective:The cytokine B-cell activating factor of the TNF family (BAFF) is involved in the pathogenesis of autoimmune diseases. We assessed changes in serum protein and mRNA level of BAFF after rituximab treatment.
Methods:Serum and peripheral blood mononuclear cells (PBMCs) were isolated from 5 patients (2 with lupus, 2 with Sjögren’s syndrome, 1 with rheumatoid arthritis) before and 12 weeks (range 7 to 17) after a first course of rituximab infusion. Monocytes and B cells were selected from healthy controls and co- cultured for 72 h. BAFF protein and mRNA levels were assessed by ELISA and real-time PCR, respectively.
Results:After rituximab treatment, median serum BAFF protein level significantly increased as well as BAFF to actin mRNA ratio in PBMCs. In monocytes co- cultured with autologous B cells, BAFF protein level decreased, whereas the mRNA level was stable. In 1 patient closely monitored, the mRNA ratio of BAFF to actin in PBMCs increased later than BAFF serum level.
Conclusions:Two distinct mechanism are probably involved in BAFF level increase after B-cell depletion: first, the decrease in its receptors leading to a release of BAFF; second a delayed regulation of BAFF mRNA transcription. This could favor the re-emergence of autoreactive B cells.
- Sjögren's syndrome
- rheumatoid arthritis