Fig. 1.

Neuro–immune crosstalk in the skin. a Imiquimod induces skin inflammation by enhancing CGRP secretion from TRPV1+ sensory neurons. CGRP promotes dendritic cell-derived IL-23 production and then activates γδ T cells to produce IL-17 and IL-22. b SADBE activates TRPV1+ sensory neurons to release CGRP, which in turn inhibits the secretion of inflammatory cytokines from dermal macrophages. c S.aureus stimulates TRPV1+ sensory neurons to secrete CGRP, leading to suppression of macrophage inflammation and lymphocyte proliferation. d Streptococcus pyogenes increases TRPV1+ sensory neuron-derived CGRP release, which inhibits neutrophil recruitment. When infected with Candida albicans, TRPV1+ sensory neurons release CGRP. CGRP promotes the production of IL-23 from dermal dendritic cells, which then activates γδ T cells and exacerbates skin inflammation. e Skin injury drives the release of NAV1.8+ sensory neuron-derived CGRP. CGRP binds to RAMP1 expressed on macrophages and neutrophils, promoting tissue healing. f Cold exposure induces IL-18 production from TRPM8+ sensory neurons. IL-18 activates skin ILC2s to secrete IL-5. ILC2-derived IL-5 promotes proliferation of keratinocytes and UCP1 expression in hypodermal adipocytes, resulting in enhanced thermogenesis