Nociceptive sensory neurons drive interleukin-23-mediated psoriasiform skin inflammation
The abnormal activation of skin immune cells, such as dermal dendritic cells (DDCs) and interleukin (IL)-17-producing γδ T (γδT17) cells, by IL-23 is known to provoke psoriasis-type inflammation. What is less well known is how peripheral nerves regulate cutaneous immune responses. In this study, IL-23-dependent psoriasis-like inflammation was induced in mice to help determine the precise molecular mechanism of neuroimmune communication in the skin. Findings indicate nociceptor (TRPV1(+)Nav1.8(+)) mediated control of DDCs regulate the IL-23/IL-17 pathway and control cutaneous immune responses. The identification of the role of nociceptor sensory neurones in skin inflammation opens new avenues for the treatment of this, and other inflammatory diseases. However, it should be noted that this study only assessed findings on IL-23-dependent psoriasis-like inflammation in mice – caution should be taken translating these findings to human models.