It is well known that Th1 T cells are activated by certain interleukins (IL-12), producing proinflammatory cytokines such as IFN-γ  and TNF-a, which are involved in the mechanism of autoimmune encephalitis [78], an activation pattern believed to have caused meningoencephalitis in 6% of vaccinated patients, together with moderate-to-high levels of CD45 immunoreactivity, which may lead to enhanced phagocytosis and degradation of brain fibrillar Aß load as reported elsewhere [18, 80]. This evidence concerns the gene IFNG and autoimmune encephalitis.