Yu Zhiping, Liu Ji, Chen Letian, Xie Junping
Department of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, People's Republic of China.
Department of Respiratory and Critical Care Medicine, Yingtan People's Hospital, Yingtan, Jiangxi, People's Republic of China.
J Inflamm Res. 2025 Aug 13;18:10953-10967. doi: 10.2147/JIR.S530754. eCollection 2025.
Rheumatoid arthritis (RA) is a systemic autoimmune disorder characterized by chronic synovitis and extra-articular manifestations (EAMs), with interstitial lung disease (ILD) being a leading cause of mortality. Interleukin-6 (IL-6), a pivotal cytokine in RA pathogenesis, drives both articular and pulmonary inflammation through its involvement in immune dysregulation and fibrotic processes. This review elucidates the molecular mechanisms by which IL-6 contributes to rheumatoid arthritis-associated interstitial lung disease (RA-ILD) progression, particularly via the Janus kinases (JAK)/signal transducers and activators of transcription (STAT) signaling pathway and macrophage polarization. Additionally, we objectively evaluate current and emerging therapeutic strategies targeting IL-6 and downstream pathways.
类风湿关节炎(RA)是一种全身性自身免疫性疾病,其特征为慢性滑膜炎和关节外表现(EAM),间质性肺疾病(ILD)是主要的死亡原因。白细胞介素-6(IL-6)是RA发病机制中的关键细胞因子,通过参与免疫失调和纤维化过程,驱动关节和肺部炎症。本综述阐明了IL-6促进类风湿关节炎相关间质性肺疾病(RA-ILD)进展的分子机制,特别是通过Janus激酶(JAK)/信号转导和转录激活因子(STAT)信号通路以及巨噬细胞极化。此外,我们客观评估了针对IL-6及其下游通路的现有和新兴治疗策略。