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The experimental autoimmune encephalomyelitis (EAE) is a model of a T CD4+ lymphocyte-mediated autoimmunity disease1. T cells goes through the process of maturation, differentation and selection inside thymus, which besides other processes, should inhibit the release of autoagressive cells. Thymus is a primary organ responsible for T cell development; and despite this unique function it is a target organ in many different diseases. In this project, we aim to caracterize thymus alterations during the clinical course of EAE. Previously, we demonstrated that thymus from EAE mice, after 15 days post immunization, presented reduction in thymus relative weight, loss of cortical-medullary delimitation and loss of double positive thymocytes. Here in, we demonstrate that thymus atrophy is directly related to the clinical score of the disease and that the loss of cortical-medullary is followed by alterations in the expression pattern of molecules involved on neural transmission during the evolution of EAE. Our results add new information about thymus atrophy that might contribute to a better understanding of development of autoreactive cells in EAE as well as to further knowledge about the thymic interaction at different pathological processes.

Initial thymus characterization during the evolution of experimental encephalomyelitis