Department of Psychiatry and Behavioral Sciences, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Cousins Center for Psychoneuroimmunology, UCLA Semel Institute for Neuroscience and Human Behaviour, Los Angeles, CA, USA.
Nat Rev Rheumatol. 2023 Sep;19(9):545-559. doi: 10.1038/s41584-023-00997-3. Epub 2023 Jul 24.
Sleep has a homeostatic role in the regulation of the immune system and serves to constrain activation of inflammatory signalling and expression of cellular inflammation. In patients with rheumatoid arthritis (RA), a misaligned inflammatory profile induces a dysregulation of sleep-wake activity, which leads to excessive inflammation and the induction of increased sensitivity to pain. Given that multiple biological mechanisms contribute to sleep disturbances (such as insomnia), and that the central nervous system communicates with the innate immune system via neuroendocrine and neural effector pathways, potential exists to develop prevention opportunities to mitigate the risk of insomnia in RA. Furthermore, understanding these risk mechanisms might inform additional insomnia treatment strategies directed towards steering and reducing the magnitude of the inflammatory response, which together could influence outcomes of pain and disease activity in RA.
睡眠在免疫系统的调节中具有同定节律的作用,有助于限制炎症信号的激活和细胞炎症的表达。在类风湿关节炎(RA)患者中,炎症谱的失调会导致睡眠-觉醒活动的失调,从而导致过度炎症和对疼痛敏感性的增加。鉴于多种生物学机制导致睡眠障碍(如失眠),并且中枢神经系统通过神经内分泌和神经效应途径与先天免疫系统进行通信,因此有可能开发预防机会来降低 RA 中失眠的风险。此外,了解这些风险机制可能会提供其他失眠治疗策略,以引导和减少炎症反应的程度,从而共同影响 RA 中的疼痛和疾病活动的结果。