“…Its pathogenesis is diverse and involves a complex histaminergic and non-histaminergic pathway, where the crosstalk between the immune system, cutaneous and neuronal cells has an impact on numerous dermatological and systemic diseases. Among the known pruritogens that signal through shared Janus kinase pathways, the most important roles are played by Th2 cytokines (IL-4, IL-13, IL-31), thymic stromal lymphopoietin, periostin, substance P, neurokinin 1R, neurotrophins nerve growth factor, autotaxin, histamine H4 receptor and oncostatin M [ 42 , 43 , 44 ]. In the inflamed lesional skin of AD patients compared to healthy controls, cells of the inflammatory, including eosinophils, basophils and lymphocytes, infiltrate and have been described to release various pruritogens and through their interaction with neuronal cells, which is correlated with itch severity.…”