Mild experimental autoimmune encephalitis as a tool to induce blood-brain barrier dysfunction.

The blood-brain barrier (BBB) serves as a border limiting access of immunoglobulins from the circulation into the brain. This becomes relevant when studying the pathogenesis of antibody-mediated autoimmune CNS disorders. Here, we characterized the BBB dysfunction in a model of mild experimental adoptive transfer autoimmune encephalomyelitis (AT-EAE). We show that large molecules can readily penetrate the BBB between days 3 and 7 after EAE-induction. This model may be valuable for studying putative pathogenic effects of immunoglobulins in the central nervous system.