Patients with multiple sclerosis (MS) who are treated with fingolimod have an increased proportion of transitional B cells in the circulation, but the underlying mechanism is not known. We hypothesized that B cell-activating factor of the tumor necrosis factor family (BAFF) is involved in the process. Compared with healthy controls and untreated MS patients, fingolimod-treated MS patients had significantly higher serum concentrations of BAFF, which positively correlated with the proportions and the absolute numbers of transitional B cells in blood. Despite the elevated concentrations of BAFF in fingolimod-treated MS patients, serum levels of soluble transmembrane activator and calcium-modulating cyclophilin ligand interactor, and B cell maturation antigen were not elevated. Our results show that fingolimod induces BAFF in the circulation and expands transitional B cells, but does not activate memory B cells or plasma cells in MS, which is favorable for the treatment of this disease.

用芬戈莫德治疗的多发性硬化症（MS）患者循环中的过渡性B细胞比例增加，但是其潜在机制尚不清楚。我们假设肿瘤坏死因子家族（BAFF）的B细胞激活因子参与了该过程。与健康对照组和未经治疗的MS患者相比，芬戈莫德治疗的MS患者血清中BAFF的浓度明显更高，这与血液中过渡性B细胞的比例和绝对数量呈正相关。尽管芬戈莫德治疗的MS患者中BAFF浓度升高，但可溶性跨膜激活剂和钙调节亲环素配体相互作用物以及B细胞成熟抗原的血清水平并未升高。