세미나

Inflammatory skin diseases trigger diverse immune responses, yet how different stimuli reprogram peripheral sensory neurons over time remains unexplored at single-cell resolution. We define, by longitudinal single-cell transcriptomics with peak-phase chromatin-accessibility profiling, the reprogramming of dorsal root ganglion sensory neurons across multiple atopic dermatitis and psoriasis models, spanning the acute-to-established transition and anchored to itch behavior. We identified inflammation-remodeled neuronal clusters arising from small-diameter nociceptors—virtually absent at homeostasis yet reproducible across all models—that engage a conserved core program of synaptic plasticity, chromatin remodeling, and neuronal sensitization, mapping onto the human itch transcriptome. Atopic and psoriasiform dermatitis then diverged across population dynamics—magnitude, repertoire, and fate—and regulatory wiring: psoriasiform neurons engaged an interferon-driven potassium-channel brake coupled to resolution, whereas atopic neurons sustained an amplifier program, left this brake unengaged, and persisted as a disinhibited remodeled pool. Neuroimmune circuits within the ganglion and from the skin relayed these programs. Together, this openly available resource advances a framework in which milieu quality, not its duration, specifies whether sensory remodeling and the itch it sustains persist or resolve.