Sensory neurons are activated by physical and chemical stimuli, eliciting sensations such as temperature, touch, pain, and itch. From an evolutionary perspective, sensing danger is essential for organismal survival. Upon infection and injury, immune cells respond to pathogen/damage-associated molecular patterns (PAMPs/DAMPs) through pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs), and produce inflammatory mediators that activate sensory neurons through neuro-immune interactions. Sensory neurons also express TLRs and other PRRs that directly sense danger signals after injury or during infection, leading to pain, itch, or analgesia. In addition to slow-acting canonical TLR signaling, TLRs function uniquely in sensory neurons through non-canonical coupling to ion channels, enabling rapid modulation of neuronal activity. We discuss how sensory neurons utilize TLRs and other PRR pathways to detect danger signals in their environment.

中文翻译：

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感觉神经元如何感知危险信号？

感觉神经元被物理和化学刺激激活，引发温度、触觉、疼痛和瘙痒等感觉。从进化的角度来看，感知危险对于生物体的生存至关重要。在感染和损伤后，免疫细胞通过模式识别受体 (PRR)，如 Toll 样受体 (TLR)，对病原体/损伤相关分子模式 (PAMP/DAMP) 做出反应，并产生炎症介质，通过神经免疫激活感觉神经元相互作用。感觉神经元还表达 TLR 和其他 PRR，它们在受伤后或感染期间直接感知危险信号，从而导致疼痛、瘙痒或镇痛。除了缓慢作用的经典 TLR 信号之外，TLR 通过与离子通道的非经典耦合在感觉神经元中发挥独特的作用，从而能够快速调节神经元活动。