Even if primary roles of T cells and B cells are to maintain homeostasis in mild AD conditions, the crosstalk between glial cells and these peripheral immune cells can increase the production of proinflammatory mediators (e.g., IL-1β, IL-6, IL-12, IL-18, and TNFα), leading to neurodegeneration in severe ADs [148]. This evidence concerns the gene IL18 and Alzheimer disease.