In conclusion, we have demonstrated (i) that IL-31/IL-31RA interaction in dendritic cells under Th2-skewed conditions may increase the production of CCL17 and CCL22, contributing to the disease activity of AD, and (ii) that Glyteer treatment could have potential to prevent the production of CCL17 and CCL22 in AD (Figure 5). This evidence concerns the gene CCL22 and Alzheimer disease.