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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, the role of nociceptors in regulating sterile cutaneous inflammation remains unexplored. To address 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 not only play a crucial role in inflammation through avoidance reflexes and behaviors, but can also regulate sterile cutaneous immunity in vivo.

Original publication




Journal article


J Invest Dermatol

Publication Date





1936 - 1945.e3


Animals, Calcitonin Gene-Related Peptide, Dendritic Cells, Dermatitis, Disease Models, Animal, Diterpenes, Female, Humans, Mice, Mice, Knockout, Nerve Fibers, Neurotoxins, Nociceptors, Skin, Sunburn, TRPA1 Cation Channel, TRPV Cation Channels, Ultraviolet Rays