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.

中文翻译：

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炎性疼痛中的免疫细胞因子及其受体

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。疼痛由初级感觉神经元（伤害感受器）介导，该神经元可以响应各种热，机械和化学信号。现在公认细胞因子是炎性疼痛的重要介质。它们可以通过介体间接诱导伤害感受器敏化，其中神经元被启动，因此对刺激的反应更强。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。我们在这里回顾支持和反对这些各自机制的证据，重点是关节炎和炎症性皮肤模型。文献中得出的结论之间存在许多惊人的矛盾之处，并对此进行了讨论。