IL17A and Alzheimer disease: [41], [60], [68], [69]. Another example is Th17 in AD and ILC3 in UC.  Their IL-17 release contributes to intestinal inflammation in UC [61], and in certain AD endotypes [35] to tissue damage and chronic skin inflammation in AD [70]. Immune myeloid cells (eosinophils, neutrophils), fibroblasts, and sensory nerve endings show similar molecular activity, supporting mechanisms of tissue injury, chronic inflammation, and pain [62], [63], [64], [65].