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Background：The genetic research background of IL-4R versus IL-31 stems from its central pathological role in Th2-type immune diseases such as atopic dermatitis: IL-4R α as a key mediator of IL-4 and Il-13 signaling pathways, IL-4R α as a key mediator of IL-4 and Il-13 signaling pathways, IL-4R as a key mediator of Il-13 signaling, and IL-3R as a key mediator of Il-13 signaling, by activating downstream cascades such as Jak/STAT, which drive inflammatory factor release with skin barrier dysfunction; whereas Il-31 is secreted by activated Th2 cells, by binding to its receptor IL-31RA/OSMR β complex, IL-31RA/OSMR β is released by activated Th2 cells, direct activation of sensory neurons cause severe itching, the formation of“Inflammation-itching-scratching” vicious cycle. The sustained activation of il-4rα can induce the expression of IL-31, and then amplify the immune inflammatory response.
