Together with Th2 (IL-13, IL-31 and CCL17) activation, enhanced Th22 (IL-22 and S100As), Th17 (IL-17A, IL-19, CCL20, LL37 and peptidase inhibitor 3/elafin), and Th1 (IFN-γ and CXCL9/CXCL10/CXCL11) pathways characterize adult AD, whereas pediatric patients exhibit lower Th1 activation but a higher expression of Th9 (IL-9), and innate markers (IL-1β, IL-8 and IFN-α1), as well as dysfunctions in epidermal lipid metabolism responsible for the barrier alterations [71,72]. This evidence concerns the gene IFNG and Alzheimer disease.