Peripheral neuroimmune dialogues underlying pain states.

Peripheral neuroimmune crosstalk is a key determinant of pain states, with immune-to-neuron signalling both initiating and amplifying hypersensitivity across multiple tissues.

• Why it matters: Pain is shaped by interactions between peripheral immune mediators and nociceptors, but the field needs a unified view of shared versus tissue-specific pathways to guide translation.
• What they did: This Review synthesizes evidence that nociceptors express receptors for cytokines, lipid mediators, complement components, antibodies, and microbial signals, and that they reciprocally modulate immune and stromal cells via neuropeptides and cytokines.
• The result: It proposes that maladaptive feedback loops can reinforce hypersensitivity while coordinated signalling can also support pain resolution, and it outlines therapeutic opportunities to rebalance these pathways for mechanism-based analgesia.

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