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Increasing evidence suggests that nerve fibers responding to noxious stimuli (nociceptors) modulate immunity in a variety of tissues including the skin. Yet, a role for nociceptors in regulating sterile cutaneous inflammation remains unexplored. To tackle this question, we have developed a detailed description of the sterile inflammation caused by overexposure to UVB irradiation (i.e. sunburn) in the mouse plantar skin. Using this model, we observed that chemical depletion of nociceptor terminals did not alter the early phase of the inflammatory response to UVB, but it caused a significant increase in the number of dendritic cells and αβ T cells as well as enhanced extravasation during the later stages of inflammation. Finally, we showed that such regulation was driven by the nociceptive neuropeptide Calcitonin Gene Related Peptide. In conclusion, we propose that nociceptors do not only play a crucial role in inflammation through avoidance reflexes and behaviors but can also regulate sterile cutaneous immunity in vivo.
This article was published in the following journal.
Name: The Journal of investigative dermatology
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Clusters of neurons in the somatic peripheral nervous system which contain the cell bodies of sensory nerve axons. Sensory ganglia may also have intrinsic interneurons and non-neuronal supporting cells.
Inflammation of the choroid in which the sensory retina becomes edematous and opaque. The inflammatory cells and exudate may burst through the sensory retina to cloud the vitreous body.
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A putative protein interaction module, approximately 70 amino acids long, that forms a small five-helix bundle with two large interfaces which may homo- and hetero-oligomerize, or bind non-sterile-alpha motif targets. The sterile alpha motif is present in a wide variety of eukaryotic proteins that function in diverse biological processes.
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