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Rituximab-induced T cell depletion in patients with rheumatoid arthritis: Association with clinical response

机译:类风湿关节炎患者利妥昔单抗诱导的T细胞耗竭:与临床反应的关系

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Objective Rituximab, a monoclonal antibody specifically targeting CD20, induces B cell depletion and is effective in the treatment of rheumatoid arthritis (RA). This study was undertaken to evaluate whether routine monitoring of lymphocyte subpopulations, especially T cells, may be useful in patients receiving rituximab for RA. Methods We examined data on all RA patients receiving rituximab between July 2007 and November 2012 in our center. Peripheral blood CD3+, CD4+, CD8+, CD3-CD56+, and CD19+ lymphocyte counts before and during the first course of rituximab were measured by flow cytometry. The Mann-Whitney nonparametric test was used to compare lymphocyte subpopulation counts before and during treatment. Results Data on 52 patients were examined. Rituximab induced unexpected and substantial depletion of T cells, mainly CD4+ cells, in most patients. The CD4+ cell count decreased by a mean ± SD of 37 ± 33% as compared to baseline at week 12, reaching <200 cells/μl in 3 patients. Importantly, lack of CD4+ cell depletion was associated with no clinical response. Therefore, the mechanism of action of rituximab may depend at least in part on T cells. Conclusion Rituximab induces substantial T cell depletion, mainly of CD4+ cells, which is associated with the clinical response in RA. Routine monitoring of T cells may be useful in the clinical setting of RA.
机译:目的利妥昔单抗是一种特异性靶向CD20的单克隆抗体,可诱导B细胞耗竭,可有效治疗类风湿关节炎(RA)。这项研究旨在评估常规监测淋巴细胞亚群,特别是T细胞,对于接受利妥昔单抗治疗RA的患者是否有用。方法我们研究了2007年7月至2012年11月间所有接受利妥昔单抗的RA患者的数据。通过流式细胞术测量利妥昔单抗第一个疗程之前和期间的外周血CD3 +,CD4 +,CD8 +,CD3-CD56 +和CD19 +淋巴细胞计数。使用Mann-Whitney非参数检验比较治疗之前和治疗期间的淋巴细胞亚群计数。结果检查了52例患者的数据。在大多数患者中,利妥昔单抗诱导T细胞(主要是CD4 +细胞)的意外和大量消耗。与第12周的基线相比,CD4 +细胞计数平均降低了37±33%±SD,在3例患者中达到了<200细胞/μl。重要的是,缺乏CD4 +细胞消耗与无临床反应相关。因此,利妥昔单抗的作用机制可能至少部分取决于T细胞。结论利妥昔单抗可诱导T细胞的大量消耗,主要是CD4 +细胞的消耗,这与RA的临床反应有关。常规监测T细胞可能在RA的临床环境中有用。

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