Inflammation has been described as a deleterious factor in MS immunopathogenesis for a long time. However, recent studies have proved the neuronal protective and efficacious effects of inflammation. Inflammation in the brain is a double-edged process that may be beneficial in promoting homeostasis and repair, but can also result in tissue injury through the damaging potential of inflammatory mediators. Control mechanisms that minimize the extent of the inflammatory reaction are necessary in order to preserve brain architecture and restore function. The end result of the inflammatory process, neurotoxicity and/or neuroprotection, is a function of the fine balance between the two cellular systems and of the complex signaling relationships between anti-inflammatory neuroprotective factors. In central nervous system inflammation the extent of tissue injury depends on both native and adaptive elements of the immune system. Besides, inflammation is not limited with the invasion of exogeneus cells infiltrating from the blood brain barrier. Astrocytes and microglial cells as being endogeneous also play an important role in the process. Secondary inflammatory mediators from these cells trigger the unique local inflammation of central nervous system. In the active MS plaques distinct cytokines and chemokines have been determined.