The Experimental Autoimmune Encephalomyelitis (EAE) is the experimental model for human Multiple Sclerosis (MS). The EAE has been helping to understand the inflamatory mechanisms of the MS and to test and develop new drugs. The inflamatory response during EAE is characterized by mononuclear cells infiltration in the central nervous system (CNS) and, consequently, destruction of myelin. The EAE can be transfered to healthy animals by the injection of T CD4+ lymphocytes previously sensibilized with CNS mielin components. However, little is known about how these cells iniciate the inflamatory process. Our preliminary data show that these autoreactive T CD4+ lymphocytes have a high expression of cytotoxic molecules like granzimes B; C and perforin. These cytotoxic molecules expression could explain the direct action of the autoreactive T CD4+ lymphocytes on the demyelination caused by the inflamatory process on EAE. Therefore, our aim is to better evaluate these molecules expression during the clinical evolution of the disease and their role in the generation and mainteance of the autoreactive response during EAE.
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