Multiple sclerosis is a chronic autoimmune disorder that targets myelinated axons in the central nervous system (CNS). This results in demyelinization which leads to loss of neuronal signalization and sometimes even to neuronal death. MS is characterized by various symptoms such as sensory, visual and motor disorders, fatigue, pain and cognitive deficits. Their manifestation varies from patient to patient. MS is a multifactorial disease that can be influenced by various genetic and environmental factors, but the exact cause is still unknown. It occurs at the age of 20-40 and affects 2,5 million people worldwide. There are 4 types of MS: relapsing remitting, secondary progressive, primary progressive and progressive relapsing. MS therapies reduce the duration of acute exacerbations, their frequency and relieve symptoms, but unfortunately, they are unable to cure the disease. Since the immune system plays a central role in disease pathogenesis, all currently available therapies are immunomodulatory. The role of the immune system in pathogenesis of the disease is described in detail in this work. This work also contain an extensive overview of the mechanisms of action and efficacy of immunomodulatory cytokine IFN-β, the first MS therapy. IFN-β treatment reduces the annual relapse rate, reduces activity and progression of the disease, but generally does not have long-term effect because its clinical efficacy is decreasing over time. This work explains effects of IFN-β on transport of immune cells to the CNS, B cell activity, antigen presenting cells, T cell activity and its direct neuroprotective functions. Despite its pleiotropic effect on the immune system, IFN-β does not cure MS and neutralizing antibodies that develop in a large number of patients treated with IFN-β have been proposed as the main cause of treatment failure. IFN-β therapy has progressed with the new formulation of pegylated IFN-β that has greater clinical efficacy. There is still room for improvement of IFN-β therapy and potential ways are discussed in this work.