University of Melbourne, Department of Medicine at Royal Melbourne Hospital, Parkville, Victoria 3050, Australia.
University of Melbourne, Department of Medicine at Royal Melbourne Hospital, Parkville, Victoria 3050, Australia; Janssen-Cilag, 1-5 Khartoum Road, North Ryde, NSW 2113, Australia.
Trends Immunol. 2018 Mar;39(3):240-255. doi: 10.1016/j.it.2017.12.003. Epub 2018 Jan 12.
There is burgeoning interest in the interaction between the immune and nervous systems. Pain is mediated by primary sensory neurons (nociceptors) that can respond to a variety of thermal, mechanical and chemical signals. Cytokines are now recognized as important mediators of inflammatory pain. They can induce nociceptor sensitization indirectly via mediators, wherein neurons become primed and thus become more responsive to stimulation; alternatively, there is also evidence that cytokines can directly activate neurons via their specific receptors present on the neuronal cells. We review here the evidence for and against these respective mechanisms, focusing on arthritis and inflammatory skin models. A number of striking inconsistencies amongst the conclusions made in the literature are highlighted and discussed.
人们对免疫系统和神经系统之间的相互作用越来越感兴趣。疼痛是由初级感觉神经元（伤害感受器）介导的，这些神经元可以对各种热、机械和化学信号做出反应。细胞因子现在被认为是炎症性疼痛的重要介质。它们可以通过介质间接诱导伤害感受器致敏，使神经元被预先激活，从而对刺激更敏感；或者，也有证据表明细胞因子可以通过神经元细胞上存在的特定受体直接激活神经元。在这里，我们回顾了这些机制的证据，重点关注关节炎和炎症性皮肤模型。文献中得出的结论存在许多显著的不一致之处，我们对此进行了强调和讨论。
