Rheumatoid arthritis (RA) is a multifactorial immune disease exhibiting diverse clinical responses to specific therapeutic agents. Such heterogeneity reflects variable activation of signaling pathways. Consequently, RA physiopathology has been linked to many immune cells and factors, with controversial observations for interferons (IFNs). In this opinion article, we review the roles of these cytokines and the cells that produce them in light of recent data: clinical observations showing that expression of IFN-dependent genes does not reflect RA activity and RA mouse models in which the stimulation of IFN-dependent pathways provided disease protection. We suggest that epicutaneous stimulation of the IFN network is an attractive possibility to limit neutrophil infiltration or activation, thus providing therapeutic benefits to RA patients refractory to current therapies.

类风湿关节炎（RA）是一种多因素免疫疾病，表现出对特定治疗剂的多种临床反应。这种异质性反映了信号通路的可变激活。因此，RA生理病理学已与许多免疫细胞和因子相关联，对干扰素（IFN）的观察也颇具争议。在这篇观点文章中，我们根据最新数据回顾了这些细胞因子的作用以及产生这些细胞因子的细胞的临床观察：临床观察结果表明，IFN依赖性基因的表达不能反映RA活性以及RA小鼠模型中的IFN-依赖性途径提供了疾病保护。我们建议对IFN网络进行表皮刺激是限制中性粒细胞浸润或激活的诱人可能性，