Bellocchi Chiara, Favalli Ennio Giulio, Maioli Gabriella, Agape Elena, Rossato Marzia, Paini Matteo, Severino Adriana, Vigone Barbara, Biggioggero Martina, Trombetta Elena, Caporali Roberto, Beretta Lorenzo
Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico and University of Milan, Milan, Italy.
University of Milan and ASST PiniCTO - Presidio Gaetano Pini, Milan, Italy.
ACR Open Rheumatol. 2025 Jul;7(7):e11761. doi: 10.1002/acr2.11761. Epub 2025 May 19.
Patients with rheumatoid arthritis (RA) often fail to respond to therapies, including JAK inhibitors (JAKi), and treatment allocation is made via a trial-and-error strategy. A comprehensive analysis of responses to JAKi, including tofacitinib, by RNA sequencing (RNAseq) would allow the discovery of transcriptomic markers with a two-fold meaning: (1) an improved knowledge about the mechanisms of response to treatment (inference modeling) and (2) the definition of features that may be useful in treatment optimization and assignment (predictive modeling).
Thirty-three patients with active RA were treated with a tofacitinib dose of 5 mg twice a day for 24 weeks and evaluated for EULAR Disease Activity Score in 28 joints using the C-reactive protein level response. Whole-blood RNA was collected before and after treatment to perform RNAseq transcriptome analysis. Linear models were used to determine differentially expressed genes (DEGs) (1) at baseline according to clinical responses and (2) in the pre-post comparison after tofacitinib treatment and in relation to EULAR responses. The capability of DEGs to predict a successful treatment was tested via machine learning modeling after extensive internal validation.
Of 26 patients who completed the study (per-protocol analysis), 15 (57.7%) achieved good responses, and 7 (26.9%) and 4 (15.3%) had moderate and no responses, respectively. Overall, 273 baseline genes were significantly associated with the attainment of good responses, contributing to several pathways linked to the immune system or RA pathogenesis (eg, citrullination processes and the negative regulation of natural killer function). The expression of several molecules was reverted by tofacitinib when good responses were reached, including AKT3, GK5, KLF12, FCRL3, BIRC3, TSPOAP1, and P2RY10. Finally, we isolated 14 markers that singularly were capable of predicting the attainment of good responses, including, NKG2D, CD226, CLEC2D, and CD52.
Whole-blood transcriptome analysis of patients with RA treated with tofacitinib identified genes whose expression may be relevant in prognostication and understanding the mechanisms of responses to therapy.
类风湿关节炎(RA)患者常常对包括JAK抑制剂(JAKi)在内的治疗无反应,治疗分配采用试错策略。通过RNA测序(RNAseq)对包括托法替布在内的JAKi反应进行全面分析,将有助于发现具有双重意义的转录组标志物:(1)更好地了解治疗反应机制(推理建模);(2)定义可能有助于治疗优化和分配的特征(预测建模)。
33例活动期RA患者接受每日两次5mg托法替布治疗,为期24周,并使用C反应蛋白水平反应评估28个关节的欧洲抗风湿病联盟(EULAR)疾病活动评分。在治疗前后收集全血RNA以进行RNAseq转录组分析。使用线性模型确定差异表达基因(DEG):(1)在基线时根据临床反应;(2)在托法替布治疗前后的比较中以及与EULAR反应相关的情况。在进行广泛的内部验证后,通过机器学习建模测试DEG预测成功治疗的能力。
在完成研究的26例患者(符合方案分析)中,15例(57.7%)获得良好反应,7例(26.9%)和4例(15.3%)分别有中度反应和无反应。总体而言,273个基线基因与获得良好反应显著相关,涉及与免疫系统或RA发病机制相关的多个途径(例如瓜氨酸化过程和自然杀伤功能的负调节)。当达到良好反应时,托法替布可使几种分子的表达恢复正常,包括AKT3、GK5、KLF12、FCRL3、BIRC3、TSPOAP1和P2RY10。最后,我们分离出14个能够单独预测获得良好反应的标志物,包括NKG2D、CD226、CLEC2D和CD52。
对接受托法替布治疗的RA患者进行全血转录组分析,确定了其表达可能与预后及理解治疗反应机制相关的基因