Oriented T cell migration induces thymic atrophy in experimental autoimmune encephalomyelitis in mice

Objective To investigate the mechanisms of thymic atrophy in experimental autoimmune encephalomyelitis (EAE). Methods EAE was induced in C57BL/6 mice.The mice immunized with OVA peptide were served as control.The amount of cells were determined in thymus, spleen and lymph nodes at different time points.Thymus-derived T cells in the spleen and infiltrating cells in central nervous system(CNS) were analyzed. Results EAE with typical motor system dysfunction and monocyte infiltration in CNS was induced by MOG peptide in CFA.The number of cells in the thymus was increased, and peaked at day 5, followed by a decrease when mice were immunized with OVA or MOG peptide.From the onset of the disease (day 10), thymocytes reduced rapidly and completely lost in some cases with severe disease.After immunization, lymphocytes in spleen and dLNs, especially recently thymus-derived T cells, continuously increased prior to the onset of the disease.However, upon the mice have developed EAE, T cells in the spleen decreased rapidly, accompanied by a dramatic increase of the infiltrated lymphocytes in CNS. Conclusion Enhanced thymus T cell output and oriented T-cell migration to CNS contribute to thymic atrophy in EAE. Key words: Experimental autoimmune encephalomyelitis; Thymic atrophy; Apoptosis; Mice