A team of Harvard researchers discovered that certain nerve cells that generate the sensation of pain are linked to the inflammatory response that results in psoriasis flares.
Nerve cells drive skin inflammation by controlling the function of dermal dendritic cells (DDCs) in the skin, Lorena Riol-Blanco, PhD, from Harvard Medical School, Boston, and colleagues reported in Nature.
The skin of mice were exposed to imiquimod (Medicis), which induced interleukin 23 (IL-23)-dependent psoriasis-like inflammation. They found that a subset of sensory neurons were essential to drive this inflammatory response. Imaging of intact skin revealed that a large fraction of DDCs, which are the principal source of IL-23, is in close contact with these nociceptors. Following selective pharmacological or genetic ablation of nociceptors, DDCs failed to produce IL-23 in imiquimod-exposed skin, according to the study data.
A nociceptor is a receptor of a nerve cell that responds to potentially damaging stimuli by sending signals to the spinal cord and brain. This process usually causes the perception of pain.
The investigators concluded that certain nociceptors regulate the IL pathways and control dermal immune responses.
“These findings indicate that TRPV1+Nav1.8+ nociceptors, by interacting with DDCs, regulate the IL-23/IL-17 pathway and control cutaneous immune responses,” wrote the researchers.