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Systemic BCG infection leads to altered T-cell trafficking, thus suppressing a CNS autoimmune disease. Prior infection also reduces EAE clinical symptoms and the frequency of IFN-γ-producing MOG-specific T cells in the CNS. As a result of the chemokine and cytokine gradients generated by peripheral granuloma, activated auto-reactive T cells are diverted from their original effector sites and are detained in granuloma
