Given the multi-factorial nature of the pathogenesis of AD, it is not surprising that Th1, Th2, Th17, and Th22 lymphocytes and the cytokines they release, as well as increased IgE production, have all been implicated in dermatitis in humans [42], rodents [43,44], and canines [[45], [46], [47]]. This evidence concerns the gene IGHE and Alzheimer disease.