Hydroxychloroquine is widely used for autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis. Although B cells contribute to the pathogenesis of these diseases, the action of hydroxychloroquine on B cells remains unclear. Here we examined the effects of hydroxychloroquine on functions of B cell subsets. Hydroxychloroquine efficiently inhibited the mammalian target of rapamycin complex 1, differentiation of CD19⁺IgD⁻CD27⁺ class-switched memory B cells to plasmablasts and their IgG production, under stimulation with CpG, a Toll-like receptor (TLR)-9 ligand. Hydroxychloroquine also inhibited CpG-induced production of interleukin-6 and tumor necrosis factor-α in B cell subsets. Taken together, hydroxychloroquine markedly suppresses the TLR9-mediated human B cell functions during inflammatory processes. Based on our results, we believe that hydroxychloroquine can be beneficial in the treatment of B cell-mediated autoimmune diseases.

羟氯喹被广泛用于自身免疫性疾病，例如系统性红斑狼疮和类风湿关节炎。尽管B细胞助长了这些疾病的发病机理，但是羟氯喹对B细胞的作用仍不清楚。在这里，我们检查了羟氯喹对B细胞亚群功能的影响。羟氯喹有效抑制雷帕霉素复合物1的哺乳动物靶标，使CD19 ⁺ IgD ^- CD27 ⁺分化在Toll样受体（TLR）-9配体CpG的刺激下，类记忆B细胞转变为成浆细胞并产生IgG。羟氯喹还抑制CpG诱导的B细胞亚群中白介素6和肿瘤坏死因子-α的产生。两者合计，羟氯喹显着抑制炎症过程中TLR9介导的人类B细胞功能。根据我们的结果，我们认为羟氯喹对治疗B细胞介导的自身免疫性疾病有益。