Musculoskeletal Research Group, Institute of Cellular Medicine, Newcastle University, UK.
Ann Rheum Dis. 2012 Nov;71(11):1888-94. doi: 10.1136/annrheumdis-2011-201115. Epub 2012 Jun 26.
Personalised healthcare is contingent on the identification of biomarkers that represent disease relevant pathways and predict drug response. The authors aimed to develop a gene expression signature in synovial tissue that could enrich clinical response of rheumatoid arthritis (RA) patients to rituximab.
The authors studied synovial gene expression using high-throughput quantitative real-time-PCR in 20 RA patients who underwent arthroscopy before and after treatment with rituximab. Several objective approaches were used to explore patterns in the data and to find genes associated with changes in disease activity due to treatment.
This analysis revealed two patient populations associated with distinct clinical, laboratory and histological features and, importantly, showed enrichment for response (60% non-responders vs 90% responders). A composite baseline gene score (GS) correlated with change in disease activity score (ΔDAS) between baseline and month 3 (r=0.74, p=0.0002), but also with ΔDAS at later time-points (month 9, r=0.54, p=0.016; month 15, r=0.45, p=0.06; month 21, r=0.72, p=0.003). Notably, the GS significantly correlated with baseline erythrocyte sedimentation rate (r=0.69, p=0.0008), but not with other DAS components. The GS genes represented T cell, macrophage, remodelling and interferon-α biology. Responders demonstrated higher expression of macrophage and T cell genes, while non-responders showed higher expression of interferon-α and remodelling genes.
This study reveals a baseline synovial GS that correlates with early and late clinical responses to rituximab. The GS biology suggests that T cells and macrophages are important for response to B cell depleting therapy, while expression of remodelling and interferon-α genes correlates with poor response.
个性化医疗取决于能够代表疾病相关途径并预测药物反应的生物标志物的识别。作者旨在开发一种在滑膜组织中可富集类风湿关节炎(RA)患者对利妥昔单抗临床反应的基因表达特征。
作者使用高通量实时定量 PCR 研究了 20 例接受利妥昔单抗治疗前后行关节镜检查的 RA 患者的滑膜基因表达。采用几种客观方法来探索数据中的模式,并找到与治疗引起的疾病活动变化相关的基因。
该分析揭示了与不同临床、实验室和组织学特征相关的两种患者群体,重要的是,该分析显示对治疗反应的富集(60%无反应者与 90%有反应者)。基线复合基因评分(GS)与基线和第 3 个月之间的疾病活动评分(ΔDAS)变化相关(r=0.74,p=0.0002),但也与后续时间点的 ΔDAS 相关(第 9 个月,r=0.54,p=0.016;第 15 个月,r=0.45,p=0.06;第 21 个月,r=0.72,p=0.003)。值得注意的是,GS 与基线红细胞沉降率显著相关(r=0.69,p=0.0008),但与其他 DAS 成分无关。GS 基因代表 T 细胞、巨噬细胞、重塑和干扰素-α生物学。有反应者表现出更高的巨噬细胞和 T 细胞基因表达,而无反应者表现出更高的干扰素-α和重塑基因表达。
本研究揭示了与利妥昔单抗早期和晚期临床反应相关的基线滑膜 GS。GS 生物学表明,T 细胞和巨噬细胞对于 B 细胞耗竭治疗的反应很重要,而重塑和干扰素-α基因的表达与反应不良相关。