In the brain of AD mice, facilitated by increased BBB permeability, an increase of CD4+ and CD8+ cells linked to gliosis and amyloid pathology has been observed [91], and Th1 and Th17 cells induced microglial activation modulating phagocytic and secretory phenotype, while Th2 cells had no effect on microglial cytokine production [92]. The gene discussed is CD8A; the disease is Alzheimer disease.