Immunomodulation of Potent Antioxidant Agents: Preclinical Study to Clinical Application in Multiple Sclerosis

Multiple sclerosis (MS) is a chronic disease of the central nerve system (CNS) primarily affecting youngsters. The CNS has a potent antioxidant defense mechanism to scavenge reactive oxygen species (ROS). MS can be effectively studied in animal models with experimental autoimmune encephalomyelitis (EAE). The immunopathogenic mechanisms involved in EAE are attributed to T-cell-mediated inflammatory disease of the CNS and activation of T cells, which recruit invading inflammatory cells, such as macrophages. The activated T cells also induce astrocytes and microglia in situ to secrete cytokines, chemokines, and toxic molecules, namely, glutamate, nitric oxide (NO), and/or ROS, which in turn contribute to axonal damage. These processes are followed by complement activation and antibody-mediated phagocytosis of axons, which eventually lead to demyelination and axonal injury.