Department of Rheumatology, Guy's Hospital, London, UK.
Centre for Inflammation Biology & Cancer Immunology, Department of Inflammation Biology, School of Immunology & Microbial Sciences, King's College London, London, UK.
Nat Rev Rheumatol. 2024 Nov;20(11):671-682. doi: 10.1038/s41584-024-01155-z. Epub 2024 Sep 6.
Pain is one of the most debilitating symptoms of rheumatoid arthritis (RA), and yet remains poorly understood, especially when pain occurs in the absence of synovitis. Without active inflammation, experts most often attribute joint pain to central nervous system dysfunction. However, advances in the past 5 years in both immunology and neuroscience research suggest that chronic pain in RA is also driven by a variety of abnormal interactions between peripheral neurons and mediators produced by resident cells in the local joint environment. In this Review, we discuss these novel insights from an interdisciplinary neuro-immune perspective. We outline a potential working model for the peripheral drivers of pain in RA, which includes autoantibodies, resident immune and mesenchymal cells and their interactions with different subtypes of peripheral sensory neurons. We also offer suggestions for how future collaborative research could be designed to accelerate analgesic drug development.
疼痛是类风湿关节炎（RA）最具致残性的症状之一，但人们对此仍知之甚少，尤其是在没有滑膜炎的情况下出现疼痛时。没有活跃的炎症，专家通常将关节痛归因于中枢神经系统功能障碍。然而，在过去 5 年中，免疫学和神经科学研究都取得了进展，这表明 RA 的慢性疼痛也是由外周神经元与局部关节环境中常驻细胞产生的各种异常介质之间的各种异常相互作用驱动的。在这篇综述中，我们从跨学科的神经免疫角度来讨论这些新的见解。我们概述了 RA 疼痛的外周驱动因素的一个潜在工作模型，该模型包括自身抗体、常驻免疫和间充质细胞及其与不同亚型的外周感觉神经元的相互作用。我们还就如何设计未来的合作研究以加速镇痛药物的开发提出了建议。
