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Disruption of the Sensory System Affects Sterile Cutaneous Inflammation In Vivo

Research output: Contribution to journalArticlepeer-review

Original languageEnglish
Pages (from-to)1936-1945.e3
JournalJournal of Investigative Dermatology
Issue number9
Early online date8 Apr 2019
Accepted/In press12 Jan 2019
E-pub ahead of print8 Apr 2019
PublishedSep 2019


King's Authors


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.

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