Arthritis Res Ther. 2009;11(6):134. doi: 10.1186/ar2852. Epub 2009 Nov 24.
Treatment with the chimerical monoclonal antibody rituximab results in CD20-directed B cell depletion. Although this depletion is almost complete in the peripheral blood of nearly all patients with rheumatoid arthritis, a proportion of patients does not exhibit a clinical response. The paper by Nakou and colleagues suggests that a decrease in CD19+CD27+ memory B cells in both peripheral blood and bone marrow precedes the clinical response to rituximab. This finding adds to the emerging evidence that lack of response to rituximab is associated with persistence of B lineage cells in specific body compartments.
采用嵌合型单克隆抗体利妥昔单抗进行治疗可导致 CD20 靶向 B 细胞耗竭。尽管几乎所有类风湿关节炎患者的外周血中均几乎完全耗尽了 B 细胞,但仍有一部分患者未表现出临床应答。Nakou 及其同事的论文表明,外周血和骨髓中 CD19+CD27+记忆 B 细胞的减少先于利妥昔单抗的临床应答。这一发现进一步证明,对利妥昔单抗无应答与特定身体部位 B 细胞系的持续存在有关。