After the initial phase of immune response imbalance in AD, where alarmins, inflammasomes, epidermal and dermal antigen-presenting cells trigger type 2 inflammatory responses (innate responses with alarmins, ILC2s, and adaptive responses with cytokines IL-4, IL-5, IL -13, Il-31, in addition to the production of allergen-specific IgE), in chronic cases of AD, a dominance of Th1 and Th17 responses is gradually observed, mediated by the INFγ/TNFα axis and IL-17, respectively, while Th22 responses directed by IL-22 are also present.61 Here, IGHE is linked to Alzheimer disease.