Although IL-17 is not as predominant in AD as it is in psoriasis, studies have revealed that IL-17 can stimulate the differentiation of B cells into IgE-producing plasma cells, promote the release of IL-8, TNF-α, and TSLP, activate keratinocytes to express adhesion molecules, and modulate the Th2 immune response, thus triggering the chronic phase of AD (29–31). This evidence concerns the gene CXCL8 and Alzheimer disease.