T. gondii infection-induced neuroinflammation is characterized by an early activation of the resident glia and subsequent recruitment of circulating monocytes and effector T cells (49, 51).To determine whether the route of infection affects the development of the neuroinflammatory reponse, we compared the activation status of microglia and recruited Ly6Chi inflammatory monocytes as well as the IFNγ production by CD4 and CD8 T cells (Figure 5A). The gene discussed is CD8A; the disease is infection.