IL-18 further increases Th1 responses in both diseases: derived from keratinocytes [50] and inflammatory dendritic epidermal cells [51] in AD to enhanced IFNG production through IRAK and NFkB [52], [53], and from colonocytes [54] or dendritic cells [55] in UC, with increased IFNG production [56]. Here, IRAK1 is linked to Alzheimer disease.