Fig. 3

Neuroinflammation and synaptic impairment. According to a widely accepted pathogenic model for MS and experimental autoimmune encephalomyelitis (EAE), autoreactive B and T cells migrate in the CNS through the blood–brain barrier. At this site, microglial cells participate in the process of T cells reactivation presenting CNS antigens in association with MHC class II molecules. Immune cells trigger the neuroinflammatory process associated with MS and EAE, with the production of cytokines (such as IL-1β and TNF-α) and other soluble products of inflammation (such as ROS) capable to deeply influence neuronal transmission, potentially leading to the disruption of the main form of synaptic plasticity (LTP). In this process, microglial activation is associated with an over-expression of NADPH-oxidase, a ROS producing enzyme, which has been demonstrated to be relevant for synaptic plasticity impairment during neuro-inflammatory processes [58]