Interestingly, (i) Aβ42 peptides that associate with microglia-mediated pro-inflammatory host responses also co-activate TLR2 signaling [74,77]; (ii) microbial amyloids further induce pro-inflammatory interleukin IL-17A, a driver of NF-kB signaling and cyclooxygenase-2 activation; (iii) LPS and amyloids also induce other potent mediators of inflammatory responses such as IL-22 that direct TLR2 activation [76]; and (iv) pathologically up-regulated levels of IL-17A and IL-22 are associated with chronic inflammatory diseases including AD [41,45]. This evidence concerns the gene IL22 and Alzheimer disease.