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[Mechanisms involved in the regulation of immune response in experimental autoimmune encephalomyelitis in mice].

Multiple Sclerosis (MS) is a chronic inflammatory autoimmune disease of the central nervous system (CNS) characterized by the presence of cellular infiltrates consisting primarily of lymphocytes and macrophages and localized areas of demyelination in the CNS. MS is thought to be initiated by self-reactive CD4(+) Th1 T cells. Thus far, treatment modalities for MS are limited, with the most common acting nonspecifically on the immune system, resulting in a general immunosuppression accompanied by severe side effects. There is a large demand for developing MS therapy that particularly targets pathogenic myelin-specific T cells. Experimental allergic encephalomyelitis (EAE) is a well-characterized animal model that mimics many of the disease symptoms of MS, including the presence of cellular infiltrates and demyelination. EAE can be actively induced in genetically susceptible strains of mice, rats, and monkeys and is mediated by activated autoreactive CD4(+) T cells that are specific to MBP (myelin basic protein). The knowledge acquired using EAE allows us to better understand the pathogenesis of MS and thus manipulate particular components of the immune response in order to develop an efficient therapy.