Since the “itch-scratch” cycle in eczema depends on sensory neuron activation mediated by neuropeptides (35), we hypothesize that PRP exerts analogous neuroimmune regulation: it may inhibit IL-31-induced TRPV1 ion channel activation to reduce itch signaling, while concurrently repairing the epidermal barrier and modulating Th2/Th22 cytokine secretion to impede the chronic progression of eczema through multiple complementary pathways. This evidence concerns the gene IL31 and Eczematoid dermatitis.