IL22 and dentin dysplasia: Previous studies on atopic dermatitis similarly reported a significant upregulation of pathways involving defence mechanisms particularly against S. aureus, with increased expression levels of S100 proteins, DEFB4A, MMPs, SLPI and LTF. Nevertheless, the atopic dermatitis characteristic Th2 or type 2 signature (IL4, IL13, IL22, TSLP, CCL13, CCL17 and CCL26) [68] was absent from DD skin, despite the strong colonization by S. aureus observed in both diseases.