We focus on the biochemical, immunological and histological alterations that occur in the different stages of the development of experimental autoimmune encephalomyelitis (EAE) induced actively, passively by transference of specific T lymphocytes or suppressed by induction of immunological tolerance. EAE is a model of demyelinating disease that resemble multiple sclerosis in humans. Characterization of the biochemical, histopathological and immunological events involved in the development and/or suppression of this experimental pathology may be used in the diagnosis, prognosis and/or therapy of human disease. These studies include the following aspects:

A. Influence of the neuroendocrine system on the mechanisms of induction of the immune response in the EAE : We study the immunological mechanisms that participate in the differential induction of the EAE in Wistar rats that present different gonadal hormone levels. For this we study the actively induce EAE in aged animals comparatively with young animals and in gonadectomized animals by bilaterally surgical castration or supplementation with testosterone.

B. Suppression of the EAE : We intend to modulate the immune response in EAE in order to prevent or attenuate the neuropathological symptoms of the disease. In this study the non-toxic B subunit of Escherichia coli heat-labile toxin conjugated to myelin and neuronal antigens are administered orally to induce immunological tolerance in EAE.

C. Participation of synaptosomal antigens in the pathogenesis of EAE : Based on the immunological crossreaction between the myelin basic protein (MBP) and synapsin, these studies are designed to evaluate phenotypic and functionally antibody and T lymphocyte populations that recognizes both proteins in vivo and in vitro . We analyze the effect of antibodies and T cells lines from rats immunized with MBP or synapsin on neuronal cell cultures, synaptosomes and in assays of passive transference of EAE.

D. Rol of phosphorylation of synaptosomal proteins in the pathogenesis of EAE : Synapsins are a family of phosphoproteins that have been implicated in several neuronal functions. We study phosphorylation of synapsin I in relation to the neuropathological alterations during the induction, later recovery and/or suppression of EAE. Also the activity of T cells and antibodies involved in the pathogenesis of EAE on the phosphorylation of synapsin are investigated.