Multiple sclerosis is an inflammatory demyelinating disease of the central nervous system (CNS) whose main manifestation is the formation of lesions that result from the loss of myelin sheath around the axons of neurons and damage of axons themselves. Lesions arise as a result of action of autoreactive immune cells that infiltrate the brain crossing the blood brain barrier, which is why multiple sclerosis is considered an autoimmune disease. The cause of the disease is unknown but the prevailing opinion is that it is caused by a number of mutually non-exclusive factors, such as environmental and infectious factors in genetically predisposed individuals in whom an activation of existing autoreactive helper T lymphocytes happens with their subsequent pathogenic actions. Many insights about the mechanism of CNS damage in multiple sclerosis come from an animal model of induced autoimmunity - experimental autoimmune encephalomyelitis - which has many clinical, neuropathological and immunological features of multiple sclerosis. This model demonstrated that the activation and expansion of autoreactive TH1 and / or TH17 lymphocytes in secondary lymphoid organs leads to breaking of the blood-brain barrier by secretion of proinflammatory cytokines and other soluble factors such as matrix metalloproteinases and reactive oxygen species. Also, the brain cells activated by inflammatory products of the infiltrating white blood cells release cytokines that further contribute to the recruitment of leukocytes from the blood and breaking of the blood-brain barrier. A large number of activated TH cells and other proinflammatory cells migrate deeper into the white matter of the brain, resulting in the appearance of inflammatory lesions in which demyelination and damage to axons and oligodendrocytes occur. It is believed that activated macrophages and microglia cells which secrete oxygen and nitrogen radicals have the greatest role in axonal injury, which results with permanent clinical deficit. There is still no satisfactory treatment of multiple sclerosis; the target for treatment should be a point in the sequence of events from the turn of autoreactive cells in the pathogenic way and that comprehension highlights the importance of knowledge about the underlying disease mechanism.